J Bacteriol 2004,186(16):5496–5505.PubMedCrossRef 25. Cai W, Jing J, Irvin B, Ohler L, Rose E, Shizuya H, Kim UJ, Simon M, Anantharaman T, Mishra B, et al.: High-resolution restriction maps of bacterial artificial chromosomes constructed by optical mapping. Proc Natl Acad Sci U S A 1998,95(7):3390–3395.PubMedCrossRef 26. Glaser P, Frangeul L, Buchrieser C, Rusniok C, Amend A, Baquero F, Berche P, Bloecker

H, Brandt P, Chakraborty T, et al.: Comparative genomics of Listeria species. Science 2001,294(5543):849–852.PubMed 27. Vicente MF, Mengaud J, Chenevert J, Perez-Diaz JC, Geoffroy C, Baquero F, Cossart P, Berche P: Reacquisition of virulence Selleckchem GSK1120212 of haemolysin-negative Listeria monocytogenes mutants by complementation with a plasmid carrying the hlyA gene. Acta Microbiol Hung 1989,36(2–3):199–203.PubMed

28. Mereghetti L, Roche SM, Lanotte P, Watt S, van der Mee-Marquet N, Velge P, Quentin R: Virulence and cord blood mononuclear cells Capmatinib mw cytokine production induced by perinatal Listeria monocytogenes strains XMU-MP-1 from different phylogenetic lineages. Biol Neonate 2004,86(1):66–72.PubMedCrossRef 29. Seeliger HPR: Listeriosis. New York: Hafner Publishing Co; 1961. 30. Bille J: Epidemiology of human listeriosis in Europe, with special reference to the Swiss oubreak. In Foodborne Listeriosis. Edited by: Miller AJ, Smith JL, Somkuti GA. Elsevier, New York: Society for industrial Microbiology; 1990:71–74. Competing interests The authors declare that they have no competing interests. Authors’ contributions OG and ST carried out the molecular genetic studies, participated in the sequence alignment. AK carried out the PFGE analysis. MR and AL carried out the MLST analysis. SMR carried out the phenotypic studies. BS performed 4-Aminobutyrate aminotransferase the statistical analysis. GK carried out the optical mapping. LM and ALM participated in the design of

the study. PhV and SMR conceived of the study, and participated in its design and coordination, helped to draft the manuscript. All authors read and approved the final manuscript.”
“Background In the early eighteenth century, Linnaeus provided the first workable hierarchical classification of species, based on the clustering of organisms according to their phenotypic characteristics [1]. In The Origin of Species[2], Darwin added phylogeny to taxonomy, while also emphasizing the arbitrary nature of biological species: “I look at the term species as one arbitrarily given for the sake of convenience to a set of individuals resembling each other.” The reality and utility of the species concept continues to inform the theory and practice of biology and a stable species nomenclature underpins the diagnosis and monitoring of pathogenic microorganisms [3–5]. Traditional taxonomic analyses of plants and animals rely on morphological characteristics.

Int J Sustain High Educ 7(3):226–251CrossRef Youth Encounter on Sustainability (YES) Home page at: http://​www.​sustainability.​ethz.​ch”
“Sustainable development and academia In April 1989, I became president of the University of Tokyo and served in that capacity for 4 years. During my tenure, I argued that universities must be centers of scholarship that contribute to the sum total of human wisdom on a level that transcends disciplinary distinctions, such as between science and the humanities.

Repotrectinib molecular weight Toward that end, I fought for increases in research spending and improvements to the research and education facilities at Japan’s universities, which were in poor condition at the time.

In 1995, the Japanese government implemented the Basic Law on Science and Technology and followed up in 1996 with the Science and Technology Basic Plan. This plan, which is revised every 5 years, has helped spur SB525334 mw a dramatic increase in competitive Cyclosporin A in vivo funding and other outlays for science and technology research. Even so, research and education in Japan still face many problems. First of all, funding for the humanities and social sciences is far too meager. If we are to contribute to the advancement of humanity, we must encourage the balanced development of both the hard sciences and the humanities, for which the latter area in particular requires more investment. Second, funding remains woefully insufficient for education on all levels—primary, secondary, and higher. From the standpoint of long-term policy for our nation, substantive improvement in this area should be a major priority for Japan. The University of Tokyo, like other universities, has recently seen criticism

aimed at the ‘reductionist’ fragmentation of academic disciplines, with many voices calling for a merging of the sciences and humanities. While I strongly advocate balanced development in both areas, I personally consider it impossible for any one individual to master the entire spectrum of knowledge. Rolziracetam Therefore, I think it is unrealistic to expect all students and researchers to gain a comprehensive knowledge of both the sciences and humanities. What I do hope is that scholars in either area will acquire a certain degree of familiarity with the other. At universities, this can be achieved by requiring a minor as well as a major of students. For this same reason, is it not unrealistic to envision a generation of sustainable development ‘specialists’ whose perspective simultaneously encompasses the entire field? What research for sustainable development demands is, if anything, increasingly specialized work by experts in such fields as energy, food, and water; however, they must also be capable of collaborating in the overall effort to solve global environmental problems.

NS = Not significant. C. Oral inoculations of Balb/c mice with EGD-e::pIMC3kan #see more randurls[1|1|,|CHEM1|]# and EGD-e InlA m * ::pIMCery mixed

at a 1:1 ratio in a total inoculum of 1 × 1010 cfu/200 μl containing 100 mg of CaCO3. *** = p < 0.005. D. Competitive index virulence in a Balb/c oral infection model with EGD-e InlA m * ::pIMC3ery competed against EGD-e::pIMC3kan, EGD-e A::pIMC3kan (InlA-N259Y), EGD-e B::pIMC3kan (InlA-Q190L), EGD-e C::pIMC3kan (InlA-T164A/K301I/G303E) or EGD-e D::pIMC3kan (InlA-S173I/L185F/L188I) as described in C. The invasion levels were significantly (p < 0.005) different than EGD-e InlA m * for all competed strains. Figure 8 Bioluminescent imaging (BLI) of Balb/c mice orally infected with either EGD-e or EGD-e InlA m* (tagged with pIMK2 lux ). A. Balb/c mice (five per group) were gavaged with a total of 5 × 109 cfu and the progression of infection in each mouse (labelled 1 thru 5) followed on day one, two and three by BLI. Pseudocolor overlay represents the light emission profile from the infected mice with the scale bar on the right hand side. On day three mice were euthanized selleck chemical and livers examined ex vivo by BLI. B. Total bacterial loads from livers and spleens were numbered. The cross line denotes the mean organ cfu recovery for the five mice.

Statistical analysis was conducted using a student t test with the p-value shown on the graph. Discussion It is now well established that the murine model of listeriosis is limited by a poor interaction between the bacterial invasion protein InlA and its host ligand mCDH1. This is in direct contrast, to the efficient interaction between InlA and hCDH1. The discrepancy is due to a glutamate at residue 16 in mouse (and rat) E-cadherin rendering these host species relatively resistant to infection by the oral route and limiting their use

as laboratory models for certain L. monocytogenes-mediated disease processes [11]. Recent studies have developed an engineered mouse strain expressing ‘humanized’ E-cadherin for studies of oral and fetoplacental listeriosis [14]. An alternative approach has utilized structure-based ifenprodil engineering to ‘murinize’ the bacterial InlA protein in order to increase affinity for murine E-cadherin [17]. This approach has provided key insights into the interaction between InlA and CDH1. While murinization was highly successful, we reasoned that additional points of contact may also improve the interaction with mCDH1. We therefore developed a system to select random mutations in InlA that enhance invasion of murine cells in order to identify novel amino acid interactions and to determine if ‘murinization’ of the strain can be improved. L. lactis was used as a surrogate host for this process in order to prevent generation of Listeria mutants with increased affinity for human cells.

J Parasitol 2005, 91:269–274.PubMedCrossRef 15. Afrin F, Ali N: Adjuvanticity and protective immunity elicited

by Leishmania donovani antigens encapsulated in positively charged liposomes. Infect Immun 1997, 65:2371–2377.PubMed 16. Bhowmick S, Ravindran R, Ali N: Leishmanial antigens in liposomes promote protective immunity and provide immunotherapy against visceral leishmaniasis via polarized AZD3965 Th1 response. Vaccine 2007, 25:6544–6556.PubMedCrossRef 17. Bhowmick S, Ravindran R, Ali N: gp63 in stable cationic liposomes confers sustained vaccine immunity to susceptible BALB/c mice infected with Leishmania donovani . Infect Immun 2008, 76:1003–1015.PubMedCrossRef 18. Bhowmick S, Ali N: Identification of novel Leishmania donovani antigens that help define correlates of vaccine-mediated protection in visceral leishmaniasis. PLoS One 2009, 4:e5820.PubMedCrossRef 19. PLX-4720 ic50 McMahon-Pratt D, Alexander J: Does the

Leishmania major paradigm of pathogenesis and protection hold for New World cutaneous leishmaniases or the visceral disease? Immunol Rev 2004, FDA-approved Drug Library purchase 201:206–224.PubMedCrossRef 20. Engwerda CR, Murphy ML, Cotterell Sara EJ, Smelt Sara C, Kaye PM: Neutralization of IL-12 demonstrates the existence of discrete organ-specific phases in the control of Leishmania donovani . Eur J Immunol 1998, 28:669–680.PubMedCrossRef 21. Kaye PM, Curry AJ, Blackwell JM: Differential production of Th1 and Th2-derived cytokines does not determine the genetically controlled or vaccine induced rate of

cure in murine visceral leishmaniasis. J Immunol 1991, 146:2763–2770.PubMed 22. Melby PC, Yang J, Zhao W, Perez LE, Cheng J: Leishmania donovani p36(LACK) DNA vaccine is highly immunogenic but not protective against experimental visceral leishmaniasis. Infect Immun 2001, 69:4719–4725.PubMedCrossRef 23. Miralles GD, Stoeckle MY, McDermott DF, Finkelman FD, Murray HW: Th1 and Th2 cell-associated cytokines in experimental visceral leishmaniasis. Infect Immun pentoxifylline 1994, 62:1058–1063.PubMed 24. Murray HW, Hariprashad J, Coffman RL: Behavior of visceral Leishmania donovani in an experimentally induced T helper cell 2 (Th2)-associated response model. J Exp Med 1997, 185:867–874.PubMedCrossRef 25. Satoskar A, Bluethmann H, Alexander J: Disruption of the murine interleukin-4 gene inhibits disease progression during Leishmania mexicana infection but does not increase control of Leishmania donovani infection. Infect Immun 1995, 63:4894–4899.PubMed 26. Alexander J, Carter KC, Al-Fasi N, Satoskar A, Brombacher F: Endogenous IL-4 is necessary for effective drug therapy against visceral leishmaniasis. Eur J Immunol 2000, 30:2935–2943.PubMedCrossRef 27. Mazumdar T, Anam K, Ali N: A mixed Th1/Th2 response elicited by a liposomal formulation of Leishmania vaccine instructs Th1 responses and resistance to Leishmania donovani in susceptible BALB/c mice.

However, when these indices have been used to assess the ability of dietary supplements to enhance click here recovery after heavy eccentric

exercise, they have been unable to detect a treatment effect [10, 13]. Muscle soreness, assessed by the subjective pain rating in the present study, is one of the most commonly used measures of exercise-induced muscle injury [2]. However, Warren et al. [2] suggested that soreness correlates poorly with muscle function. In the current study, the patterns of recovery for hanging joint angle, relaxed arm circumference, and subjective pain ratings were similar in the ANA and PLA conditions (Figure 3b). Therefore, the lack of effect of supplementation on the hanging joint angle and relaxed AZD6738 ic50 arm circumference in these studies [10, 13], the poor correlation between muscle function and soreness [2], and the results of the present study have collectively suggested that these indicators of muscle damage may not be sensitive to dietary supplement interventions to improve recovery from eccentric-induced muscle BIBW2992 research buy damage. Future studies may wish to consider these

findings when selecting outcome variables for assessing the efficacy of dietary supplementation for reducing muscle damage. A secondary objective of this study was to examine the effects of 10 days of ANA dietary supplementation on resting heart rate and blood pressure. As a minor alkaloid with a similar chemical structure to nicotine, we hypothesized that Anacetrapib ANA would cause moderate decreases in systolic and diastolic blood pressure and small increases in resting heart rate. Previous studies [14, 26, 27] have shown that acute nicotine exposure causes an increase heart rate and blood pressure through stimulation of the sympathetic nervous system. Minami et al. [28] showed that smoking cessation caused a reduction in heart rate, which implied that chronic nicotine use may elevate heart rate. However, cross sectional studies [26,

29] have shown that systolic and diastolic blood pressures are lower in smokers than in non-smokers. The results of the present study indicated that, over a period of 10 days, ANA had no effect on heart rate or blood pressure compared to placebo. Thus, ANA supplementation may be safe regarding short-term use (10 days) on resting heart rate and blood pressure. However, future studies may wish to examine the acute and chronic effects of ANA consumption on blood pressure and heart rate to further discern its safety. Conclusions In conclusion, ANA supplementation had no effect on the recovery of muscle strength, hanging joint angle, arm swelling, or subjective pain ratings after a bout of maximal eccentric exercise in the forearm flexors. Therefore, ANA may not be beneficial for those seeking to improve recovery from heavy exercise training or competition.

Renal function was already decreased by age 20, at least in hypertensive children [20]. The important finding in the present study is that declining rates of eGFR and increasing rates of TKV are not significantly different between normal blood pressure and high blood pressure patients after around 20 years. This phenomenon might or might not be due to anti-hypertensive treatment. The results of previous [20] and present studies suggest that renal functional deterioration starts

far earlier than 20 years of age, especially in hypertensive ADPKD patients. The potential limitations of this study include retrospective analysis, use of eGFR and 1/Cr, as well as an ethnically homogenous patient population in Japan, and hence it may not be applicable to other ethnicities. Conclusions In learn more conclusion, eGFR starts to decline in young adult patients with apparently normal eGFR. After A-1155463 molecular weight adolescence, the declining rate of eGFR is relatively constant and does not relate to age or GFR. Hypertensive patients had lower eGFR and larger Sepantronium TKV than normotensive patients at young adult age. After adolescence, eGFR declined at a similar rate between normotensive and hypertensive groups. A long-term longitudinal study

starting in childhood is necessary to more thoroughly understand the characteristics of disease progression in ADPKD. Acknowledgments This study was supported in part by a Grant-in-Aid for Progressive Renal Diseases Research from the Ministry of Health, Labor and Welfare of Japan. Conflict of interest Dr. Higashihara serves as consultant to Otsuka Pharmaceutical. Open Access This article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are Farnesyltransferase credited. Electronic supplementary material Below is the link to the electronic supplementary material. 1/Creatinine is plotted against age in all 255 patients (JPEG 87 kb) References 1. Franz KA, Reubi FC. Rate of

functional deterioration in polycystic kidney disease. Kidney Int. 1983;23:526–9.PubMedCrossRef 2. Grantham JJ, Chapman AB, Torres VE. Volume progression in autosomal dominant polycystic kidney disease: the major factor determining clinical outcomes. Clin J Am Soc Nephrol. 2006;1:148–57.PubMedCrossRef 3. Grantham JJ, Torres VE, Chapman AB, Guay-Woodford LM, Bae KT, King BF Jr, Wetzel LH, et al. Volume progression in polycystic kidney disease. N Engl J Med. 2006;354:2122–30.PubMedCrossRef 4. Meijer EM, Rook M, Tent H, Navis G, van der Jagt EJ, de Jong PE, et al. Early renal abnormalities in autosomal dominant polycystic kidney disease. Clin J Am Soc Nephrol. 2010;5:1091–8.PubMedCrossRef 5. Helal I, Reed B, McFann K, Yan X, Fick-Brosnahan GM, Cadnapaphornchai M, et al.

The elemental composition of the Zr/CeO x /Pt was determined by energy dispersion. The results from the EDX analysis that showed the main component

present in this structure were O (38.41%), Zr (34. 05%), and Ce (3.83%). An oxygen peak at about 0.52 keV and Zr peaks at about 22.5 and 15.60 keV can be observed in the spectra. Figure 1 XRD pattern of the CeO x film and cross-sectional TEM selleckchem and EDX images of the Zr/CeO x /Pt device. (a) XRD pattern of the CeO x film deposited on Si wafer at room temperature. (b) Cross-sectional TEM image of the Zr/CeO x /Pt device. (c) EDX image of the Zr/CeO x /Pt device. The ZrO y layer is also observed from XPS signals at the interface of Zr and CeO2 layers. XPS analysis

was carried out to examine the surface chemical composition and the valence/oxidation states of Ce and Zr species involved in the device by inspecting the spectral line shape and signal intensities associated with the core-level electrons. Figure 2a shows the depth profile of chemical composition in the Zr/CeO x /Pt device. The interdiffusion of O, Ce, and Zr atoms are evident from the spectra. This is an indication of the formation of an interfacial ZrO y layer between the CeO x and Zr top electrode. The formation of the ZrO y layer is further confirmed from the shifting of Zr 3d peaks from a higher binding energy Selleckchem 4SC-202 position to lower ones (Figure 2c). The CeO x 3d spectrum shown in Figure 2b consists of two sets of spin-orbit multiplets. These multiplets are the characteristics of 3d3/2 and 3d5/2 (represented BCKDHA as u and v, respectively) [15]. The spin-orbit splitting is about 18.4 eV. The highest peaks at around 880.2 and 898.7 eV, recognized as v 0 and u 0 respectively, correspond to Ce3+ with the highest satellites as v′ (885.1 eV) and u′ (903.3 eV). Low-intensity peaks, i.e., v (882.5 eV) and u (900.9 eV) along with satellite features represented as v″ (889.4 eV), v‴ (897.5 eV), u″ (905.4 eV), and u‴ (914.6 eV), are observed, corresponding to the Ce4+ state. Figure 2 XPS binding energy profiles. (a)

Depth profiles of Zr, Ce, O, Pt, and W for the W/Zr/CeO x /Pt structure, (b) Ce 3d, (c) Zr 3d, and (d) O 1 s in the Zr/CeO x /Pt device. In CP673451 manufacturer reference to the differentiation between the Ce3+ and Ce4+ species with different line shapes, the XPS spectra correspond to various final states: Ce(III) = v 0 + v′ + u 0 + u′ and Ce(IV) = v + v″ + v‴ + u + u″ + u‴ [16]. The presence of the Ce4+ state is normally supported by the intensity of the u‴ peak, which is known as a fingerprint of Ce(IV) states [16]. This result implies that both Ce4+ and Ce3+ ions coexist in the bulk as well as in the surface of the CeO x film. Concentrations of Ce4+ and Ce3+, as obtained from the deconvoluted XPS spectra, are 39.6% and 60.4%, respectively.

‡‡ Good, better, bad and worse refer to the buy CHIR-99021 comparisons between treatments in terms of their clinical risks and benefits. ††† Good reference standards are independent of the test, and applied blindly or objectively to applied to all patients. Poor reference

standards are haphazardly applied, but still independent of the test. Use of a OSI-027 nmr non-independent reference standard (where the ‘test’ is included in the ‘reference’, or where the ‘testing’ affects the ‘reference’) implies a level 4 study. †††† Better-value treatments are clearly as good but cheaper, or better at the same or reduced cost. Worse-value treatments are as good and more expensive, or worse and

the equally or more expensive. ** Validating studies test the quality of a specific diagnostic test, based on prior evidence. An exploratory study collects information and trawls the data (e.g. using a regression analysis) to find which factors are ‘significant’. *** By poor learn more quality prognostic cohort study we mean one in which sampling was biased in favour of patients who already had the target outcome, or the measurement of outcomes was accomplished in <80% of study patients, or outcomes were determined in an unblinded, non-objective way, or there was no correction for confounding factors. **** Good follow-up in a differential diagnosis study is >80%,

with Digestive enzyme adequate time for alternative diagnoses to emerge (for example 1-6 months acute, 1 – 5 years chronic) Table 3 Grading system for ranking recommendations in clinical guidelines Grade of recommendation   A Good evidence to support a recommendation for use B Moderate evidence to support a recommendation for use C Poor evidence to support a recommendation, or the effect may not exceed the adverse effects and/or inconvenience (toxicity, interaction between drugs and cost) D Moderate evidence to support a recommendation against use E Good evidence to support a recommendation against use Results – Definition, risk factors, natural history and diagnosis Patients with ASBO treated nonsurgically have shorter hospital stay, however they have an higher recurrence rate, shorter time to re-admission, although the risk of new surgically treated episodes of ASBO is the same.

In the context of the inconsistent profiles between tissue-based and plasma-based result, however, some consistently reported miRNAs in tissue-based profiling studies, for example, a panel of miR-21, miR-210 and miR-486-5p, have been validated in plasma-based studies to confirm their diagnostic value in the diagnosis CP-690550 mouse of lung cancer with solitary pulmonary nodules [39]. Future studies that based on parallel plasma and tissue samples may provide more solid evidence. For the included profiling studies in which adjacent corresponding normal lung tissue served as an expression baseline, we need to know that adjacent appearing

morphologically normal tissue may contain molecular changes associated with cancer [40, 41]. Third, rigorous validation and demonstration of reproducibility

in an independent population are necessary to confirm the predictive value of miRNAs. One of the most frequently investigated miRNAs is miR-21, it ranks second among consistently reported up-regulated miRNAs in this meta-analysis, it has been also reported to be associated with prognosis in several kinds of cancer [42–44]. From the prognostic point of view, AZD0156 nmr over expression of miR-21 has been reported to be independently associated with reduced survival of pancreatic ductal adenocarcinoma [43]. High miR-21 expression was also associated with poor survival of colon adenocarcinoma in both the training cohort (US test cohort of 84 patients with incident colon adenocarcinoma, recruited between 1993 and 2002) and validation cohort (independent Chinese cohort of 113 patients recruited between 1991 and 2000) [44]. However, when expression of miR-21, miR-29b, miR-34a/b/c, miR-155, and let-7a was determined by quantitative real-time PCR in formalin-fixed paraffin-embedded tumor specimens from 639 patients who participated in the International Adjuvant Lung Cancer Trial (IALT), there was a deleterious borderline prognostic DNA Synthesis inhibitor effect of lowered miR-21 expression [45]. Conclusions In conclusion, the top

two most consistently reported up-regulated miRNAs were miR-210 and miR-21. The results of this meta-analysis of human lung cancer miRNA expression profiling studies might provide some clues of the potential biomarkers in lung cancer. Further mechanistic and external validation studies are needed for their clinical significance and role in the development of lung cancer. Acknowledgements This work was supported by Key Laboratory Project, Liaoning Provincial Department of Education (No. LS2010168) and the National Natural Science Foundation of China (No. 81102194). The funding sources had no role in the study Copanlisib chemical structure design, data collection, analysis and interpretation, or in the writing of this manuscript. References 1.

The ionic redistributions were in agreement with subsequent measurements, conducted in collaboration with a postdoc from Germany (Gottfried Wagner), including agreement with respect to a small chloride influx (Chow CP673451 clinical trial et al. 1976). However, the large chloride influx observed in a Tris buffer (Hind et al. 1974) puzzled us; to explain it quantitatively, our model assumed a certain concentration of protonated Tris+ cations sequestered in the thylakoid lumen because of the light-induced ΔpH, the Tris+ cations acting like Donnan fixed charges (Chow et al. 1976). Electron transport, proton translocation and photophosphorylation were to occupy Alex’s attention

for the rest of career. Thus, he attempted to estimate the proton motive force (PMF) in thylakoids (Hope et al. 1982a), making the first observations of the effects of ionophores on the PMF and photophosphorylation concurrently (Hope et al. 1982b). He further refined the estimation of the trans-thylakoid ΔpH by correcting for the binding of the amine probe used (Hope and Matthews 1985). Applying the correction to the estimates of ΔpH, he then compared ΔG ATP (the ‘phosphorylation potential’) with ΔG H+ (the

free energy difference between protons in the aqueous bulk phases inside and outside). The results could not be reconciled with a simple, SBE-��-CD supplier bulk-phase chemiosmotic relationship selleck screening library unless the electric potential difference was up to +155 mV (Hope et al. 1985), an unreasonably high value for thylakoids. The authors concluded that the PMF may not be poised at all times in relation to the phosphorylation potential as required by the macrochemiosmotic concept, and that the results did not rule out the microchemiosmotic

concept involving localized protons or its variations. Their conclusion is consistent with the observation that the rate of ATP synthesis declined in an abrupt fashion on cessation of illumination with or without valinomycin, even though the ΔpH declined with Oxalosuccinic acid much more slowly (Chow et al. 1978). Proton deposition in the lumen was resolved into three phases (Hope and Matthews 1984): a fast phase (<1 ms, not resolved) which is usually attributed to protons from oxidation of water; an intermediate phase (ca. 3 ms), usually attributed to the oxidation of plastoquinonol, which showed a damped, binary periodicity very like that for proton uptake (Hope and Matthews 1983); and a slow phase (70–90 ms) which may have its origin near PS II. The intermediate phase of proton deposition led Alex to study the kinetics of electron and proton transfers around the cytochrome (cyt) b/f complex where oxidation of plastoquinonol occurs: modelling the constraints on Q-cycle activity (Hope and Matthews 1988); measuring the rate of cyt b-563 reduction (Hope et al. 1989); and kinetically resolving the proton uptake associated with turnover of the quinone-reduction site (Hope and Rich 1989).