scholarly journals Tryptophan Derivatives by Saccharomyces cerevisiae EC1118: Evaluation, Optimization, and Production in a Soybean-Based Medium

2021 ◽  
Vol 22 (1) ◽  
pp. 472
Author(s):  
Michele Dei Cas ◽  
Ileana Vigentini ◽  
Sara Vitalini ◽  
Antonella Laganaro ◽  
Marcello Iriti ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Kynurenic Acid ◽  
Potential Role ◽  
Defined Medium ◽  
The Other ◽  
Chemically Defined Medium ◽  
Cultural Medium ◽  
Whole Cell Biotransformation ◽  
Tryptophan Derivatives

Given the pharmacological properti es and the potential role of kynurenic acid (KYNA) in human physiology and the pleiotropic activity of the neurohormone melatonin (MEL) involved in physiological and immunological functions and as regulator of antioxidant enzymes, this study aimed at evaluating the capability of Saccharomyces cerevisiae EC1118 to release tryptophan derivatives (dTRPs) from the kynurenine (KYN) and melatonin pathways. The setting up of the spectroscopic and chromatographic conditions for the quantification of the dTRPs in LC-MS/MS system, the optimization of dTRPs’ production in fermentative and whole-cell biotransformation approaches and the production of dTRPs in a soybean-based cultural medium naturally enriched in tryptophan, as a case of study, were included in the experimental plan. Variable amounts of dTRPs, with a prevalence of metabolites of the KYN pathway, were detected. The LC-MS/MS analysis showed that the compound synthesized at highest concentration is KYNA that reached 9.146 ± 0.585 mg/L in fermentation trials in a chemically defined medium at 400 mg/L TRP. Further experiments in a soybean-based medium confirm KYNA as the main dTRPs, whereas the other dTRPs reached very lower concentrations. While detectable quantities of melatonin were never observed, two MEL isomers were successfully measured in laboratory media.

scholarly journals The Grand Challenge of Corporate Control: Opening strategy to the normative pressures of networked professionals

2020 ◽  
Vol 1 (4) ◽  
pp. 263178772096969
Author(s):  
Richard Whittington ◽  
Basak Yakis-Douglas
Keyword(s):  
Potential Role ◽  
Corporate Control ◽  
Labour Markets ◽  
The Other ◽  
Grand Challenge ◽  
Big Business ◽  
Research Themes ◽  
The One ◽  
Open Strategy

We propose that the pre-eminent ‘grand challenge’ for organization theorists today is the societal control of powerful corporations. This grand challenge is the more urgent because of the contemporary inadequacies of markets, hierarchies and regulations as instruments of control. We argue for the potential role of ‘open strategy’ in mobilizing normative controls over big business. We develop a distinction between the managed and unmanaged practices of open strategy. Both can help expose corporations to normative pressures, but we highlight the unmanaged open practices of collective subpolitics and individualist whistleblowing. Especially when mobilized by globally networked professionals, these unmanaged practices can subject corporations to normative pressures where markets, hierarchies and regulations fail. We propose two broad research themes relevant to the effectiveness of managed and unmanaged practices of strategic openness: on the one hand, there are material issues to do with labour markets, organizing and technologies; on the other hand, there are discursive questions of authenticity, capability and identity.

Preliminary Studies on Bemitradine-Induced Cardiotoxicity in Female Rats

1991 ◽  
Vol 10 (5) ◽  
pp. 511-523 ◽  
Author(s):  
S. Levin ◽  
D. Semler ◽  
S. Gad ◽  
E. Burton ◽  
G. Walsh ◽  
...  
Keyword(s):  
Potential Role ◽  
The Other ◽  
Female Rats ◽  
Separate Experiment ◽  
Direct Effects ◽  
Primary Metabolite ◽  
T Wave ◽  
Mixed Function Oxidases ◽  
Circulating Levels

The mechanism of bemitradine (SC-33643) cardiotoxicity in female rats was investigated in the set of preliminary experiments reported here. Specifically, the involvement of bemitradine metabolites and the potential role of adrenal epinephrine release were examined. Desethylbemi-tradine (the primary metabolite of bemitradine) was shown to be cardiotoxic at oral dosages greater than 300 mg/kg for 7 days. In a separate experiment, a major metabolite (bemitradine glycol) unique to the rat was not cardiotoxic at dosages up to 600 mg/kg for 7 days. Treatment of rats with SKF 525-A enhanced the lethality and the cardiotoxicity of bemitradine. In contrast, prior treatments of rats with phenobarbital resulted in decreased cardiotoxicity of both bemitradine and desethylbemitradine (a bemitradine metabolite presumably further metabolized by the microsomal mixed function oxidases). In other independent experiments, bemitradine-induced cardiotoxicity was shown to be accompanied by adrenal damage and decreases in adrenal epinephrine. Propranolol (a β-antagonist) treatment protected rats against cardiotoxicity. Bemitradine also had a direct effect on the heart, as evidenced in an experiment in which bemitradine caused dose-related increases in the T-wave of the rat ECG complex. These data suggest that (1) both bemitradine and desethylbemitradine may be responsible for the cardiotoxicity, and the other downstream metabolites are not and (2) cardiotoxicity may be due to the combination of direct effects of bemitradine on the rat heart and the bemitradine-mediated release of adrenal epinephrine (a known cardiotoxin at high circulating levels).

scholarly journals Kynurenic acid and cancer: facts and controversies

2019 ◽  
Vol 77 (8) ◽  
pp. 1531-1550 ◽  
Author(s):  
Katarzyna Walczak ◽  
Artur Wnorowski ◽  
Waldemar A. Turski ◽  
Tomasz Plech
Keyword(s):  
Kynurenic Acid ◽  
Molecular Mechanisms ◽  
Potential Role ◽  
Cancer Cell Proliferation ◽  
Gastrointestinal Microbiota ◽  
Tryptophan Metabolite ◽  
Peripheral Cells ◽  
The Relationship ◽  
The Brain

Abstract Kynurenic acid (KYNA) is an endogenous tryptophan metabolite exerting neuroprotective and anticonvulsant properties in the brain. However, its importance on the periphery is still not fully elucidated. KYNA is produced endogenously in various types of peripheral cells, tissues and by gastrointestinal microbiota. Furthermore, it was found in several products of daily human diet and its absorption in the digestive tract was evidenced. More recent studies were focused on the potential role of KYNA in carcinogenesis and cancer therapy; however, the results were ambiguous and the biological activity of KYNA in these processes has not been unequivocally established. This review aims to summarize the current views on the relationship between KYNA and cancer. The differences in KYNA concentration between physiological conditions and cancer, as well as KYNA production by both normal and cancer cells, will be discussed. The review also describes the effect of KYNA on cancer cell proliferation and the known potential molecular mechanisms of this activity.

Schistosoma mansoni: evidence for a role of serum factors in protecting artificially transformed schistosomula against antibody-mediated killing in vitro

Parasitology ◽  
1978 ◽  
Vol 77 (2) ◽  
pp. 225-233 ◽  
Author(s):  
C. A. P. Tavares ◽  
Rita C. Soares ◽  
P. M. Z. Coelho ◽  
G. Gazzinelli
Keyword(s):  
Schistosoma Mansoni ◽  
Protective Factor ◽  
Gel Filtration ◽  
Defined Medium ◽  
Rabbit Serum ◽  
Chemically Defined Medium ◽  
Lethal Effects ◽  
Serum Factors

SummaryArtificially transformed schistosomula of Schistosoma mansoni develop a consistent but small protection against the lethal effects of antibody plus complement when cultured for 24 h in a chemically defined medium. In contrast, they become rapidly resistant to antibody plus complement, when cultured in the presence of a complex medium consisting of equal parts of heat-inactivated rabbit serum and Earle's/lactalbumin or in defined medium supplemented with small amounts of heat-inactivated rabbit serum. Sephadex G-200 gel filtration revealed that the protective factor in rabbit serum is a macromolecule with a molecular weight between 7 and 19S. Parasites cultured at 10 °C or in the presence of 200 μg of puromycin show less serum-induced protection against the lethal effects of antibody plus complement than do controls.

Effects of PGF2α and indomethacin on ovulation and steroid production in the isolated perfused rabbit ovary

1983 ◽  
Vol 104 (2) ◽  
pp. 233-239 ◽  
Author(s):  
Paul V. Holmes ◽  
Per O. Janson ◽  
Jan Sogn ◽  
Björn Källfelt ◽  
William J. LeMaire ◽  
...  
Keyword(s):  
Ovulation Induction ◽  
Defined Medium ◽  
The Other ◽  
Chemically Defined Medium ◽  
Perfusion Medium ◽  
Steroid Production ◽  
Experimental Side ◽  
Series Of Experiments

Abstract. Both ovaries of 31 rabbits were perfused with a chemically defined medium in vitro in a recirculation system. In one series of experiments, hCG (100 IU) was injected iv 5–6 h prior to anaesthesia and surgery. Approximately 1 h later the perfusion was started. One ovary was perfused as control while the other ovary was perfused with 5 μg/ml indomethacin or with indomethacin and 1 μg/ml PGF2α. In another series of experiments the rabbits received no pretreatment prior to operation. Instead, bovine LH was added to the perfusion medium of both control and experimental ovaries. The experimental side also received either indomethacin or indomethacin and PGF2α. Finally, the effect of PGF2α in the absence of LH was compared to the control ovary receiving only LH. After injection of hCG in vivo, ovulations occurred in 4 of 5 control ovaries. Indomethacin completely blocked ovulation in 4 of the 5 ovaries treated, while PGF2α restored ovulations in all the experimental ovaries. In the group of experiments where LH was added in vitro, ovulations were induced in all ovaries treated with varying LH doses. Furthermore, indomethacin blocked ovulation in 5 out of 7 ovaries, and PGF2α restored ovulation in all ovaries. Fifty per cent of the ovaries treated only with PGF2α (in the absence of LH) also ovulated. The pattern of steroid release did not differ between control ovaries, indomethacin treated ovaries, and indomethacin + PGF2α treated ovaries. Ovaries treated in perfusion with PGF2α alone had very low steroid levels compared to the ovaries treated with LH. This study confirms that indomethacin blocks ovulation in the perfused rabbit ovary and that this blockade can be overcome by exogenous PGF2α. Indomethacin and PG-treatments after ovulation induction did not affect ovarian steroidogenesis. Furthermore, while PGF2α was able to induce ovulations in these perfused oestrous ovaries in the absence of LH, it did not stimulate steroidogenesis.

scholarly journals Mask-Induced Priming and the Negative Compatibility Effect

2008 ◽  
Vol 55 (2) ◽  
pp. 133-141 ◽  
Author(s):  
Petroc Sumner
Keyword(s):  
Opposite Direction ◽  
Compatibility Effect ◽  
Alternative Explanation ◽  
Potential Role ◽  
The Other ◽  
Motor Inhibition ◽  
Positive Priming ◽  
Motor Activation ◽  
Random Line

Abstract. Under certain conditions, masked primes have produced counter-intuitive negative compatibility effects (NCE), such that RT is increased, not decreased, when the target is similar to the prime. This NCE has been interpreted as an index of automatic motor inhibition, triggered to suppress the partial motor activation caused by the prime. An alternative explanation is that perceptual interactions between prime and mask produce positive priming in the opposite direction to the prime, explaining the NCE without postulating inhibition. Here the potential role of this “mask-induced priming” was investigated in two experiments, using masks composed of random lines. Experiment 1 compared masks that included features of the primes and targets with masks that did not. The former should create more mask-induced priming, but the NCE did not differ between masks. Experiment 2 employed masks that contained features of either one target or the other, but not both. These asymmetric masks produced significant mask-induced priming, but it was insufficient in size to account for the prime-related NCE. Thus mask composition can contribute to NCEs, but when random line masks are employed, the major source of the NCE seems to be motor-inhibition.

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