Of these, ALS3 and HWP1 appear to play the most prominent role in biofilm development [11, 19, 35],

and evidence https://www.selleckchem.com/products/gm6001.html suggests that their differential expression could play a role in mediating detachment events [19]. We found that BCR1 was necessary for establishment of adhesion of the C. albicans biofilm to the silicone elastomer surface and that ALS3 was necessary for establishment of firm adhesion, while HWP1 was not required. Although there was a slight trend of decreased expression of TEC1 in the time course analysis, there was no indication that BCR1 was differentially EPZ015938 cost regulated during detachment and overexpression of ALS3 had only a modest effect on the detachment phenotype. The time course analysis indicated that the detachment process coincided with differential regulation of a relative abundance of genes coding for plasma membrane proteins, cell surface proteins and cell wall proteins, with a modest enrichment in these categories (data not shown). These genes were scrutinized more closely for clues that would indicate

changes in cell surface properties related to detachment. Genes involved in transport (ALP1, TNA1, CTR1, GNP1, HGT1, HGT15, and DUR7) were highly represented indicating a shift in metabolism. CBL0137 price There was no clear trend indicating that these transcripts were generally either increased or decreased during the time course. There was a general decrease in transcripts for genes involved in hyphal penetration (RAC1, PLB1) which is suggestive of a response to reject surface association. It would be reasonable to expect that induction of release from the surface would involve cell wall restructuring and two genes (SCW11, XYL2) are related to this function. Patterns of gene expression uncovered by K means analysis indicated that genes involved in similar biological processes were regulated together which provides some support for the hypothesis that the detachment process was associated with some form of coordinated transcriptional regulation. Genes involved in DNA

packaging (HTB1, HTA1, HHF22, HHT2, and NHP6a) and host interaction (RAS1, SAP5, ALS1, and TEC1) were generally down regulated (groups 1 and 7, respectively), while genes involved in carbohydrate/glycoprotein Immune system (CWH8, PSA2, and TPS3) biosynthetic processes and energy derivation/generation of precursor metabolites (TPS2, MRF1, and ADH5) were generally up regulated (groups 3 and 5, respectively). Among group 1 there were a number of genes coding for histones that were found to be differentially regulated by the quorum sensing agents farnesol or tyrosol (HTA1, HHT2, and NHP6a), both of which have been shown to influence biofilm development [43, 44]. There are a substantial number of genes whose expression levels have been shown previously to influence C. albicans biofilm formation.

New requirements for manuscripts submitted to biomedical journals have been proposed, including full declaration of potential conflicts of interest (both financial and non-financial), defined criteria for authorship and a description of the contribution made by each author [4]. In addition, editors may request that authors of a study funded by industry confirm

full access to all data used in the study and acceptance of responsibility for the accuracy Napabucasin solubility dmso and integrity of those data. The obligation to register all clinical trials and to consider seriously publication of negative studies is stressed. Although these recommendations have not yet been universally adopted they provide an important step towards constructive management of conflicts of interest in medical publishing and protecting the credibility of biomedical research. Policies to manage conflicts of interest in academic centres, teaching hospitals, research institutions and professional medical or scientific organizations have also been proposed [5–7]. Some measures have already been widely implemented, for example prohibition of acceptance of gifts from industry, removal of direct industry influence in medical education and in the development of clinical guidelines, and clearly defined institutional policies on conflicts of interest.

Company funding for attendance of buy TSA HDAC healthcare professionals at meetings has been substantially SPTLC1 reduced and strict rules are in place for the permitted standards of travel and accommodation. Industry sponsored symposia are now almost exclusively PF-3084014 conducted through intermediary continuing medical education (CME) organisations that are charged with ensuring high educational standards and avoidance of commercial bias and promotional content. More draconian proposals include a move towards a complete ban on industry funding for professional medical associations and on funding for satellite symposia at regional or national meetings. Stringent controls over research funding from industry have been recommended

and include restricting the participation of individuals with conflicts of interest in research involving human subjects [7]. Managing conflicts of interest in members of committees that develop clinical guidelines and in officers and board members of professional organisations has also received attention [3, 7]. Recent proposals recommend that individuals with any financial tie to industry should be excluded from membership of committees that formulate practice guidelines or outcome measures. The concern that this strategy will limit the expertise available to such groups is acknowledged, with the minor concession that members with conflicts of interest might play a limited role in exceptional circumstances.

To determine possible find more synergistic combinations, the effects of TAI-1 in combination with various cytotoxic drugs were evaluated. TAI-1-sensitive cancer cells were treated with an appropriate ratio of doses of cytotoxic agents to TAI-1 determined by corresponding DNA Damage inhibitor drug GI50, as shown in Table 3 (Drug 1: TAI-1 GI50 ratio) and MTS assay used to determine cellular proliferation. Combination index (CI) was calculated from the GI50s obtained to represent additive (CI = 1), synergistic (CI < 1) or antagonistic (CI > 1) effects. TAI-1 was synergistic with doxorubicin, topotecan, and paclitaxel, but not synergistic with sorafenib and the

novel src inhibitor KX-01 [15] (Table 3). Table 3 Synergistic effects of TAI-1 with cytotoxic agents Drug buy P505-15 Cell lines Drug 1 GI50(nM) TAI-1 GI50(nM) Drug 1: TAI-1 GI50ratio Combination index Synergy Doxorubicin K562 36 44 0.83 0.66 Yes MDA-MB-468 27 34 0.80 0.87 Yes Huh7 183 84 2.17

0.73 Yes Topotecan MDA-MB-231 347 43 8.01 0.78 Yes MDA-MB-468 11 34 0.32 0.74 Yes Paclitaxel Huh7 94 84 1.11 0.28 Yes MDA-MB-231 5 42 0.12 0.68 Yes K562 10 41 0.24 0.73 Yes Sorafenib Huh7 (liver) 4501 84 53.38 1.66 Antagonistic Hep3B (liver) 3676 104 35.50 1.50 Antagonistic KXO1 Huh7 (liver) 27 84 0.32 1.31 Additive *Combination index: 1 = additive, < 1 = synergy, > 1 = antagonistic. Role of RB and P53 in TAI-1 cellular sensitivity TAI-1 is active on a wide spectrum of cancer cell lines; however, 5 cell lines were resistant Nintedanib (BIBF 1120) to TAI-1 (Table 1). To explore possible resistance mechanisms of TAI-1, we evaluated the role of retinoblastoma protein RB (a Hec1 interacting protein [4, 16] through which Hec1 was discovered), and P53, another oncogene in the same category as RB, which might provide a cellular escape mechanism. The RB and P53 tumor suppressors are both critical players in DNA damage checkpoint [17]. A cross-tabulation comparison of the RB [17–22] and

P53 [20, 22–28] gene status versus sensitivity to TAI-1 (in this case, response is identified as GI50 of < 1 μM, n = 19) revealed an interesting pattern of response to Hec1 inhibitor TAI-1 (Table 1). To quantitate Hec1 protein expression levels, we analyzed the expression levels of the Hec1 protein by western blotting and quantitated protein levels using HeLa as standard, and high expression determined as > 50% HeLa expression levels. As shown in Figure 6, cell lines showing a good cellular proliferative response to TAI-1 (as defined by GI50 < 1 μM) had a much higher level of expression of Hec1 compared with resistant cell lines (GI50 > 1 μM) (p < 0.0001). Table 4 shows the relationship between the expression of Hec1 and the status of the markers. High level expression of Hec1 was associated with a better response to the Hec1 inhibitor TAI-1 (16/16 of High Hec1 expression were sensitive compared to 1/3 of the low Hec1 expression cell lines, p < 0.01). Figure 6 TAI-1 GI 50 s correlates with Hec1 protein expression in cancer cell lines.

25 ml of DPPHs and 5 ml of glycine solution with LQ   Each mixture was put in the reaction container of the electric discharge generator and exposed to electric discharge for 55 min. Every 5 min, the electric discharge apparatus was stopped, 2 ml of the solution was pipetted, put in the disposable cuvette and its UV–VIS spectra was collected. After the data acquisition, the content of the cuvette was put back in the reaction container and the electric discharge apparatus was BIX 1294 chemical structure turned back on. Reaction

Products Assessment Infrared spectral data was collected using a commercial Bruker FTIR-ATR spectrometer (Alpha equipped with Platinum ATR QuickSnapTM sampling module with a diamond ATR crystal for solids and liquids, A220/D-01). Spectral range was set to 4,000–400 cm−1, number of scans—128, as a background a clean ATR crystal was used. Experiments were performed for both amino acids separately with LQ LDN-193189 ic50 in the reaction container and the blank test was performed using glycine without quartz. Reaction mixture was exposed to electric discharge for 70 min and every 10 min approx. 0.5 ml of the solution was pipetted and measured using FTIR-ATR spectrometer. After 70 min, the samples were filtered, in order to eliminate the quartz from the solution, and dried at room temperature and pressure. Resulting crystals were also analysed on the FTIR-ATR device. Data Treatment All infrared spectra were analysed

and handled using OPUS 6.0 and EssentialFTIR software. No ATR corrections for dispersion and depth penetration were performed—the outcome data were not compared to any standard FTIR spectra. Presented PF477736 spectral plots were created using Origin 8.6. UV–VIS spectra were analysed using Specwin32. Results and Discussion Free Radicals Free radical formation in all of the reaction mixtures was proven by DPPH bleaching. With time, the value of both maxima of absorption bands in UV–VIS spectra decreases gradually (Online Resource 1, S.M. 2), therefore it can be assumed that the reaction of DPPH recombination

is strictly time-dependent. In order to compare the rates of DPPH bleaching in each mixture, reaction rate constants were calculated, assuming first-order reaction kinetics. Values of both absorption maxima are strictly correlated, the results for band at 540 nm are presented here. All spectra 3-mercaptopyruvate sulfurtransferase were fitted manually (as in Online Resource 1, S.M. 3). Absorption values were determined using program functionality. Reaction rate constant (k) was calculated using Eq. 1. $$ \mathrmIn\frac\mathrmI\mathrmI_0=-2\mathrmkt $$ (1) Equation 1 Rate constant calculation. I – absorbance instantaneous value, I 0 – absorbance value at t = 0, t – time [s] \( \ln \frac\mathrmI\mathrmI_0 \) values plotted against time are presented in Fig. 2. Highest rate of reaction is represented by mixture of quartz and glycine (6.6 · 10−3[s−1]) nearly two times lower rate is obtained for the blend of water with quartz (3.

11 Data are mean (SD) as continuous variable; number (percent) as Anlotinib categorical variable. Lumbar spine (L2–L4) and total proximal femur BMD were measured by dual-energy X-ray absorptiometry (DXA). The manufacturers of DXA equipment used at the three

geographic sites are Norland XR-26 Mark II (Fort Atkinson, WI, USA), Hologic QDR 4500C (Bedford, MA, USA), and GE-Lunar Prodigy (Madison, WI, USA) for NTUH, CCH, and NCKUH, respectively a p value indicates difference between the isoflavone and placebo groups assessed by two-sample t test bThere were 145 participants in the isoflavone group check details and 142 participants in the placebo group BMD bone mineral density, METs metabolic equivalents The efficacy of isoflavone on bone Table 2 shows the serum concentrations of genistein and daidzein. The serum concentrations of isoflavones were remarkably elevated in the isoflavone group (p < 0.001). Table 3 shows the mean percentage changes (95% CI) from their corresponding baseline values for lumbar spine (L2–L4) and total femur BMD. The differences between the isoflavone and placebo groups were not Trichostatin A statistically significant at any time point according to two-sample t tests. Using a GEE model, the differences in mean percentage changes of BMD at lumbar spine (p = 0.42) and total femur (p = 0.39) between the isoflavone and placebo groups after controlling for time effect still depicted no significant difference, respectively. However,

there was significant bone loss at the two sites in both treatment groups (p < 0.001). In the 2-year study period, both groups lost approximately 1.5% of spine BMD and 1.0% of total femur BMD. Because biases may persist in pooled BMD data from different instruments, we also analyzed mean percentage change from baseline lumbar spine and total femur BMD derived from each center. The result failed to reveal any significant

difference between the isoflavone and placebo groups (Table 4). There was no statistically significant difference in serial percentage changes of bone markers between the two groups according to two-sample t tests (Table 5). Again, using a GEE method, the difference in the serial percentage changes of BAP and urinary NTx/creatinine Rucaparib datasheet from their corresponding baselines failed to show any statistical significance between the isoflavone and placebo groups (p = 0.78 and 0.43, respectively). Table 2 Mean (SD) of serum genistein and daidzein concentrations at each visit Variable and group Baseline (N) 4 weeks (N) 48 weeks (N) 96 weeks (N) Genistein (μ mol/L)  Isoflavone 0.34 (1.26) (212) 6.85 (5.05) (210) 4.10 (4.34) (204) 3.30 (3.18) (200)  Placebo 0.23 (0.74) (211) 0.19 (0.71) (210) 0.20 (0.67) (203) 0.24 (0.80) (198)  Difference (95% CI) 0.11 (−0.08, 0.31) 6.66 (5.96, 7.35) 3.91 (3.30, 4.51) 3.05 (2.60, 3.51)  p value 0.80 <0.001 <0.001 <0.001 Daidzein (μ mol/L)  Isoflavone 0.09 (0.36) (212) 1.44 (1.35) (212) 1.12 (1.16) (204) 0.73 (0.92) (200)  Placebo 0.05 (0.20) (211) 0.07 (0.35) (211) 0.10 (0.48) (203) 0.04 (0.

​ch3 CrossRef Turconi S, Weber N, Schweitzer G, Strotmann H, this website Holzwarth AR (1994) Energy transfer and charge separation kinetics in photosystem I. 2. Picosecond fluorescence study of various PS I particles and light-harvesting complex isolated from higher plants. Biochim Biophys Acta 1187:324–334. doi:10.​1016/​S0006-3495(93)81552-2 CrossRef van Metter RL (1977) Excitation energy transfer in the light-harvesting chlorophyll a/b LY333531 nmr protein. Biochim Biophys Acta 462:642–658. doi:10.​1016/​0005-2728(77)90107-4 CrossRefPubMed van Oort B, Amunts A, Borst JW, van Hoek A, Nelson N, van Amerongen H, Croce R (2008) Picosecond fluorescence

of intact and dissolved PSI-LHCI crystals. Biophys J 95:5851–5861. doi:10.​1529/​biophysj.​108.​140467 CrossRefPubMed van Oort B, Alberts M, de Bianchi S, Dall’Osto L, Bassi R, Trinkunas G, Croce R, van Amerongen H (2010) Effect of antenna-depletion in photosystem II on excitation energy transfer in Arabidopsis thaliana. Biophys J 98:922–931. doi:10.​1016/​j.​bpj.​2009.​11.​012 selleck inhibitor CrossRefPubMed Vasile’v S, Wiebe S, Bruce D (1998) Non-photochemical quenching of chlorophyll fluorescence in photosynthesis. 5-Hydroxy-1,4-naphthoquinone in spinach thylakoids as a model for antenna based quenching mechanisms. Biochim Biophys Acta 1363:147–156. doi:10.​1016/​S0005-2728(97)00096-0 CrossRef Visser NV, Westphal AH, van Hoek A, van Mierlo CPM, Visser AJWG, van Amerongen H (2008) Tryptophan-tryptophan energy migration

as a tool to follow apoflavodoxin folding.

Biophys J 95:2462–2469. doi:10.​1529/​biophysj.​108.​132001 CrossRefPubMed Williams WP (1998) The physical properties of thylakoid membrane lipids and their relation to photosynthesis. In: Siegenthaler PA, Murata N (eds) Advances in photosynthesis. Lipids in photosynthesis. Kluwer, Dordrecht, pp 103–118 Witt HT (1979) Energy conversion in the functional membrane of photosynthesis. Analysis by light pulse and electric pulse methods. The central role of the electric field. Biochim Biophys Acta 505:355–427. doi:10.​1016/​0304-4173(79)90008-9 PubMed Yan H, Zhang P, Wang C, Liu ZH, Chang W (2007) Two lutein molecules in LHCII have different Farnesyltransferase conformations and functions: insights into the molecular mechanism of thermal dissipation in plants. Biochem Biophys Res Commun 355:457–463. doi:10.​1016/​j.​bbrc.​2007.​01.​172 CrossRefPubMed”
“Alex Hope was for many years a Foundation Professor of Biology in Biophysics and later Emeritus Professor at The Flinders University of South Australia. Throughout his career he strove to understand the energetics of plant cells, and devoted the latter two-thirds of his research career to the study of photosynthesis. His earlier, highly successful, research had focused on electrical properties and ionic relations of plant cells. The change of research direction, however, was only an apparent one, since a continuing theme was the role of electrochemical potential gradients in energy capture and conversion.

This discrepancy may be due to differences of experimental processing, regional disparity or technical issues. In our study, expression of ERCC1 in stage III + IV was higher than stage I + II (P = 0.006). This was also happened in lymph node metastasis compared to no metastasis (P AZD9291 = 0.01), which like Ota et al. reported [20]. The available data indicate ERCC1 positive patients might present a poor prognosis, and ERCC1 expression might appear

to be an advanced stage event. The BAG-1, as an anti-apoptotic function, exhibits positive expression in many malignant tumors. It binds to the cytosolic domain of the growth factor receptors on the cell surface, enhancing the protection from cell death triggered by these receptors. However, it binds to Bcl-2 and heat shock protein (HSP) and modulates their function in the selleck compound cytosol, and it binds to nuclear hormone receptors for inhibiting hormone-induced apoptosis in the nucleus [21]. Further exploration shows overexpression of BAG-1 suppresses activation of caspases and apoptosis induced by chemotherapeutic agents [22]. As expected, experiment performed in lung cancer cells indicates silencing of BAG-1 gene can sensitize lung cancer cells to cisplatin-induced apoptosis

[5]. In this study, the positive BAG-1 expression correlated significantly with progression-free and overall buy GANT61 survival in patients treated by platinum. P-type ATPase As we described, current

research has proven expression of BAG-1 indicates poor prognosis [23]. Whereas, Rorke et al. [24] reported high expression of BAG-1 may correlate to better prognosis in NSCLC. The difference between findings may be due to different choices of treatment and different components of data. BRCA1 is implicated in NER, which was discussed in the part of ERCC1, it also associates with double-strand break repair and mismatch repair, indicating its crucial role in DNA repair [25]. It has been indicated that BRCA1 presents different sensitivity to different chemotherapy agent in vitro study. The negative expression of BRCA1 results in high sensitivity to cisplatin, whereas its positive expression increases sensitivity to antimicrotubule agents [26]. In clinical research, it was found that patients whose tumors had BRCA1 expression would have significantly poorer survival and should be candidates for adjuvant chemotherapy [27]. Median survival was 11 months for 38 patients with low BRCA1, treated with cisplatin plus gemcitabine; 9 months for 40 patients with intermediate BRCA1, treated with cisplatin plus docetaxel; and 11 months for 33 patients with high BRCA1, treated with docetaxel alone. Two-year survival was 41.2%, 15.6% and 0%, respectively, which had manifested the potential predictive role of BRCA1 in a recent non-randomized phase II clinical trial [28].

Furthermore Defactinib clinical trial all the strains were susceptible to Cefalotin and Vancomycin. Phenotypic characterization of bacteria-producing slime Among the 17 isolated E. faecalis, 12 strains (71%) were slime producers developing almost black, black or very black colonies on the CRA plate and the remaining 5 strains were non-producers developing red or bordeaux colonies (Table 2). Table 2 Biofilm formation and of oral Enterococci and their adherence to abiotic and biotic surfaces Strains Identification Origin Phenotypes on CRA Slime production Mean OD595 ± SD *OD595 Adherence               Hep-2 A 549 B347 E. faecalis Caries active

AB Epigenetics inhibitor Producer 0.152 0.003 + Moderately Moderately B342 E. faecalis Caries active Black Producer 0.955 0.045 +++ Strongly Strongly B358 E. faecalis Caries active Brd Non-producer 0.224 0.008 + Strongly Strongly B403 E. faecalis Caries active AB Producer 0.360 0.011 ++ Strongly Strongly B310 E. faecalis Caries active AB Producer 0.853 0.009 +++ Strongly Strongly B281 E. faecalis Caries active AB Producer 0.508 0.018 +++ Strongly Strongly B312 E. faecalis Caries active Black Producer 0.750 0.008 +++ Strongly Strongly GDC-0973 concentration B345 E. faecalis Caries active AB Producer 0.550 0.026 +++ Strongly Strongly

B54 E. faecalis Caries active Black Producer 0.367 0.052 ++ Strongly Strongly B’381 E. faecalis Caries active Brd Non-producer 0.429 0.002 ++ Strongly Strongly B9 E. faecalis Caries active Brd Non-producer 0.391 0.002 ++ Strongly Strongly B366 E. faecalis Caries active Black Producer 0.211 0.004 + Moderately Weakly B362 E. faecalis Caries active Brd Non-producer 0.261 0.017 + Strongly Moderately B385 E. faecalis Caries active AB Producer 0.244 0.075 + Strongly Moderately B361 E. faecalis

Caries active AB Producer 0.290 0.249 + Moderately Moderately B368 E. faecalis Caries free Brd Non-producer 0.202 0.008 + Strongly Strongly B412 E. faecalis Caries free AB Producer 0.291 0.011 + Strongly Moderately B336 E. faecium Caries active Red Non-producer 0.228 0.001 + Strongly Strongly B346 E. faecium Caries active Brd Non-producer 0.181 0.003 + Moderately Moderately B577 E. faecium Caries active Very Black Producer 0.179 0.035 Nabilone + Moderately Moderately B215 E. faecium Caries free AB Producer 1.238 0.011 +++ Strongly Strongly *Biofilm production: -: non-producer (OD570 < 0.120); +: weak producer (0.120 < OD570 < 0.240; ++: producer (0.240 < OD570 < 0.5); +++: high producer (OD570 > 0.5). Among the 4 E. faecium, 2 strains were slime producers developing almost black (B215) and very black colonies (B577) on the CRA plate. Semi quantitative adherence assay All the examined strains were biofilm producers using the semi quantitative adherence assay (Table 2) and the OD570 were above 0.12, i.e. the value recognized as the limit under which strains were considered non-producers [24].

Results obtained could help to better

define strategies for pathogenicity studies and control strategies in C. perfringens and can moreover be used to design focused wet-lab experiments. Table 1 Genomes and plasmids analyzed C.p. Strain Type (name) Sequencing Status N Genes Length (nt) Str. 13 G Finished 2905 3085740 ATCC 13124 G Finished 3066 3256683 ATCC 3626 G Draft 3427 3896305 C JGS1495 G Draft 3254 3661329 CPE F4969 G Draft 3118 3510272 D JGS1721 G Draft 3485 4045016 E JGS1987 G Draft 3729 4127102 SM101 G Finished 2748 2921996 C. perfringens P (pBCNF5603) Finished 36 36695 C. perfringens P (pCP8533etx) Finished 63 64753 F4969 P (pCPF5603) Finished 73 75268 F5603 P (pCW3) Finished 51 47263 F5603 P (pCPF4969) Finished 62 70480 SM101 P (1) Finished Necrostatin-1 cost 10 12397 SM101 P (2) Finished 11 12206 Str. 13 P (pCP13) Finished 63 54310 List of genomes and plasmids used in

this study. The Type column indicates if a sequence is a genome (G) or a plasmid (P) in that case we also indicate the name of the plasmid within round parentheses. C.p. stands for Clostridium perfringens. Results and Discussion Comparisons of C. perfringens strains As a preliminary analysis we studied the variability of the selected genomes using both standard VX-680 nmr phylogenetic techniques and a comparison of all intergenic sequences. The alignment of rrnA operons for a total of 4719 nt was used to build a Neighbor-Joining tree revealing that these strains are closely related [Additional file 1: panel a]. In agreement with a low differentiation on ribosomal operon sequences, bootstrap support for the branching pattern was quite low; in fact, 32 variable sites only were found in the alignment,

which were evenly distributed between strains [Additional file 1: panel b]. However, the comparison of a large number of intergenic sequences extracted from the genomes revealed that some of them are quite variable between the different strains with respect to the very buy PRI-724 conserved rrnA operon (down to 82% with respect to C. perfringens Str. 13, [Additional file 1: panel PJ34 HCl c]). Regulon prediction in sequenced C. perfringens strains The presence of VirR and VirS sequences was checked in all strains using blast and the functionally characterized sequences of Str. 13 as queries. We found that they are indeed both present in all strains and that they are moreover always organized in what resembles a bi-cistronic operon with the two genes often overlapped (data not shown). We scanned available C. perfringens genomes using the VirR position weight matrix (PWM) derived from experimental observations, following the procedure reported in figure 1 (see Methods for details). At the time we performed this analysis (April, 2009), the NCBI microbial genome database stored three different complete genomes for C.

My undergraduate research in organic chemistry under Professor T.D. Stewart at the University of California at Berkeley involved the synthesis and study of trinitrotriphenylmethane. One purpose was to provide Professor Gilbert ROCK inhibitor N. Lewis and his postdoctoral collaborator, Glenn T. Seaborg, this compound for their study on the color of molecules. The acidity of its central hydrogen interested Lewis, much in the same way as it did my

teacher, Linus Pauling at Caltech, Pasadena (see Kalm 1994). In basic solution, a gorgeous blue salt forms and is soon oxidized on exposure to oxygen. My own research involved a study on the kinetics of oxidation of the trinitrotriphenylmethane salt in acetonitrile solution. I preserved some of this blue solution by sealing a flask of it; it has been stable for over 60 years!

eFT-508 Further organic synthetic research from 1939 to 1942 at Caltech provided more experience with the reactions of organic molecules of carbon-12. After presentation of my thesis work, Linus Pauling asked me to write the equation for the kinetics of decay of a radioactive isotope on the black board—a subject that had no relation to my thesis or to studies at Caltech. I managed to write the generalized differential equation but Pauling said nothing about his reason for asking the question. (See Pauling (1940) for his ideas Adenylyl cyclase on The Chemical Bond.) Two weeks later I received a letter from Professor Joel Hildebrand offering me a position as Instructor in the Chemistry Department at the University of

California Berkeley, with a salary of $2,000 per year. Apparently, Pauling and Wendell Latimer, Dean of the College of Chemistry and Chemical Engineering at UC Berkeley had arranged this appointment. As an Instructor, I taught courses in synthetic organic chemistry. Clearly, Pauling and Latimer had already planned that I should work with Sam Ruben and Martin Kamen in their research on the path of carbon in photosynthesis (see Gest 2005a for Kamen; and Gest 2005b for Ruben). Sam and Martin were excellent physical chemists who found themselves in the middle of an adventure in plant biochemistry, the mechanism of carbon fixation and reduction in photosynthesis. Clearly, they needed organic chemistry expertise in their quest. At this time they were not involved in the classified research involving “atomic energy/power.” I had been made aware of nuclear fission since the morning of January 13, in 1939, when Luis Alvarez came into his 11 am AG-881 nmr physics lecture in a state of shock, engendered by the news of Hahn and Meitner’s report of their discovery of nuclear fission. This discovery had to be verified at once. That momentous morning, his lecture on optics was really an excited report of the discovery in Germany that changed the course of history.