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The paper describes the problem of finding the likelihood ratio for specific problem of stochastic system recognition in continuous time to member functions within continuous-discrete time, which depend not only on current, but also on arbitrary numbers of previous non-observable process values. [ABSTRACT FROM AUTHOR]

Prostate apoptosis response protein 4 (Par-4) also known as PRKC apoptosis WT1 regulator is a tumor suppressor that selectively induces apoptosis in cancer cells. However, its post-translational regulation by ubiquitin-mediated proteolysis and the cellular machinery that is responsible for its proteasomal degradation are unknown. Using immunopurification and an unbiased mass spectrometry-based approach, we show that Par-4 interacts with the SPRY-domain containing E3 ubiquitin ligase Fbxo45 through a short consensus sequence motif. Fbxo45 interacts with Par-4 in the cytoplasm and mediates its ubiquitylation and proteasomal degradation. Fbxo45 silencing results in stabilization of Par-4 with increased apoptosis. Importantly, a Par-4 mutant that is unable to bind Fbxo45 is stabilized and further enhances staurosporine-induced apoptosis. Co-expression of Fbxo45 with Par-4 protects cancer cells against Par-4-induced apoptosis. Our studies reveal that Fbxo45 is the substrate-receptor subunit of a functional E3 ligase for Par-4 that has a critical role in cancer cell survival. [ABSTRACT FROM AUTHOR]

The paper proposes a Markovian approach to the performance evaluation of the ESSE (early slow start exit) modification of the TCP congestion control mechanism. ESSE takes advantage of estimating the optimal pipesize at the sender side to properly select initial slow start threshold. Previous simulative experiments have shown that ESSE allows one to speed-up TCP connections and significantly reduces the packet drop rate at the bottleneck. This work takes a step further in understanding the ESSE behavior by developing a model of TCP source to evaluate the influence of different settings of slow start threshold on a TCP performance. As confirmed by comparison with simulations, the model provides, significantly faster than simulations, accurate estimates of typical performance indicators such as the average completion time and average drop rate of short-lived TCP connections. [ABSTRACT FROM AUTHOR]

RASSF1A is a key tumor-suppressor gene that is often inactivated in a wide variety of solid tumors. Studies have illustrated that RASSF1A plays vital roles in the regulation of cell-cycle progression and functions as a guardian of mitosis. Nevertheless, the precise mechanism of RASSF1A-dependent regulation of mitosis remains largely unclear. APC/CCdc20 is the master switch and regulator of mitosis. The activity of APC/CCdc20 is tightly controlled by phosphorylation and specific inhibitors to ensure the sequential ubiquitination of downstream targets. Here, we report on the novel finding of a regulated circuitry that controls the timely expression and hence activity of APC/CCdc20 during mitosis. Our study showed that RASSF1A and APC/CCdc20 form a molecular relay that regulates the APC/CCdc20 activity at early mitosis. We found that RASSF1A inhibits APC/CCdc20 function through its D-box motifs. Paradoxically, RASSF1A was also demonstrated to be ubiquitinated by APC/CCdc20 in vitro and degraded at prometaphase despite of active spindle checkpoint presence. The first two unique D-boxes at the N-terminal of RASSF1A served as specific degron recognized by APC/CCdc20. Importantly, we found that Aurora A and Aurora B directly phosphorylate RASSF1A, a critical step by which RASSF1A switches from being an inhibitor to a substrate of APC/CCdc20 during the course of mitotic progression. As a result of RASSF1A degradation, APC/CCdc20 can then partially activate the ubiquitination of Cyclin A in the presence of spindle checkpoint. This circuitry is essential for the timely degradation of Cyclin A. To conclude, our results propose a new model for RASSF1A-APC/CCdc20 interaction in ensuring the sequential progression of mitosis. [ABSTRACT FROM AUTHOR]

Natural plankton communities from a tropical freshwater reservoir (Combani Reservoir, Mayotte Island, Mozambique Channel) were exposed, in 20-l nutrient-enriched microcosms, to two nominal concentrations of three pesticides: the herbicides diuron (2.2 and 11 μg/l) and paraquat (10 and 40.5 μg/l) and the insecticide fenitrothion (10 and 100 μg/l), commonly used in the tropics for agriculture and disease vector control. Bacterioplankton, phytoplankton, and zooplankton communities were monitored for 5 days after exposure, and the concentrations of toxicant and major nutrients were measured. Bacterioplankton growth was noticeable in all systems and was slightly affected by pesticide at any concentration. A transitory increase in thymidine-based bacterial production was observed in diuron- and fenitrothion-treated microcosms, followed by a marked decrease in all microcosms after 5 days. The functional diversity of bacterioplankton, evaluated using BIOLOG ECO microplates, was reduced by exposure to the highest pesticide concentrations. Phytoplankton was affected by pesticides in different ways. Chlorophyll biomass and biovolumes were increased by diuron addition and decreased by paraquat, whereas fenitrothion-treated microcosms remained unaffected relative to controls. Phytoplankton taxonomic diversity was decreased by paraquat and high doses of fenitrothion but was unaffected by addition of diuron. The decrease in diversity was due to a reduction in the number of species, whereas the density of small cells increased, especially after addition of paraquat. Heterotrophic flagellates were sensitive to paraquat and to the highest diuron concentration; a reduction in biomass of up to 90% was observed for 40.5 μg/l paraquat. Zooplankton, dominated by Thermocyclops decipiens and Diaphanosoma excisum, was slightly sensitive to diuron, and very sensitive to paraquat. High concentrations of the insecticide fenitrothion were effective only on young stages. The potential direct and indirect effects of pesticide contamination on such a simplified plankton food web, typical of newly constructed reservoirs, appear to differ significantly depending on the biological compartment considered. The overall sensitivity of tropical plankton is comparable to the sensitivity for temperate systems, and direct and indirect effects appeared rapidly, within 5 days of exposure. [ABSTRACT FROM AUTHOR]

Ecotoxicological assessment in the tropics is based mainly on knowledge gained from temperate organisms, although many studies have shown the need for models that are more appropriate to tropical regions. The toxicity of two herbicides and two insecticides to nauplii of two freshwater zooplankton species, Mesocyclops aspericornis (von Daday in Inseln Zool Jb Syst 24:175-206, ) from a tropical reservoir and a Mesocyclops sp. from a temperate pond, were compared. Both strains were sensitive to paraquat, temephos and fenitrothion, tropical M. aspericornis being generally more tolerant (EC50s of 207, 1,450 and 1,840 μg L for paraquat, temephos and fenitrothion, respectively) than the temperate Mesocyclops sp. (EC50s of 152, 45 and 1,017 μg L for paraquat, temephos and fenitrothion, respectively) whereas diuron was only slightly toxic (LOEC = 446 μg L for both strains). The nauplii mortality increased with the exposure time for both species during each experiment. Further isolation of model organisms from tropical ecosystems is needed, to meet the requirements for a tropical risk assessment scheme. [ABSTRACT FROM AUTHOR]

In B-cell chronic lymphocytic leukemia (B-CLL) cells, Lyn, a tyrosine kinase belonging to the Src family, is overexpressed and atypically localized in an aberrant cytosolic complex in an active conformation, contributing to the unbalance between cell survival and pro-apoptotic signals. In this study, we demonstrate that Lyn constitutively phosphorylates the immunoreceptor tyrosine inhibitory motifs of the inhibitory cell surface co-receptor CD5, a marker of B-CLL. As a result, CD5 provides an anchoring site to Src homology 2 domain-containing phosphatase 1 (SHP-1), a known negative regulator of hematopoietic cell function, thereby triggering the negative B-cell receptor (BCR) signaling. The subsequent segregation of SHP-1 into two pools, one bound to the inhibitory co-receptor CD5 in an active form, the other in the cytosol in an inhibited conformation, proves crucial for withstanding apoptosis, as shown by the use of phosphotyrosine phosphatase-I-I, a direct inhibitor of SHP-1, or SHP-1 knockdown. These results confirm that Lyn exhibits the unique ability to negatively regulate BCR signaling, in addition to positively regulating effectors downstream of the BCR, and identify SHP-1 as a novel player in the deranged signaling network and as a potential attractive target for new therapeutic strategies in B-CLL. [ABSTRACT FROM AUTHOR]

Ubiquitin-specific proteases (USPs) are a subclass of cysteine proteases that catalyze the removal of ubiquitin (either monomeric or chains) from substrates, thus counteracting the activity of E3 ubiquitin ligases. Although the importance of USPs in a multitude of processes, from hereditary cancer to neurodegeneration, is well established, our knowledge on their mode of regulation, substrate specificity and biological function is quite limited. In this study we identify USP47 as a novel interactor of the E3 ubiquitin ligase, Skp1/Cul1/F-box protein β-transducin repeat-containing protein (SCFβ-Trcp). We found that both β-Trcp1 and β-Trcp2 bind specifically to USP47, and point mutations in the β-Trcp WD-repeat region completely abolished USP47 binding, indicating an E3-substrate-type interaction. However, unlike canonical β-Trcp substrates, USP47 protein levels were neither affected by silencing of β-Trcp nor modulated in a variety of processes, such as cell-cycle progression, DNA damage checkpoint responses or tumor necrosis factor (TNF) pathway activation. Notably, genetic or siRNA-mediated depletion of USP47 induced accumulation of Cdc25A, decreased cell survival and augmented the cytotoxic effects of anticancer drugs. In conclusion, we showed that USP47, a novel β-Trcp interactor, regulates cell growth and survival, potentially providing a novel target for anticancer therapies. [ABSTRACT FROM AUTHOR]

Maintenance of genomic integrity is one of the fundamental biological properties shared by all living organisms. To counterbalance deleterious and potentially mutagenic effects of omnipresent DNA damaging assaults, organisms have developed a network of genome surveillance and maintenance pathways known as the DNA damage response. In eukaryotes, the orchestration of cell-cycle checkpoints, DNA damage repair, and apoptosis in response to DNA damage relies on posttranslational modifications of key regulatory proteins. Although the role of phosphorylation in these pathways is relatively well established, the significance of ubiquitylation has only recently emerged. In this review, we survey current research on the ubiquitin-proteasome system, focusing on the DNA damage response in the G2 phase of the cell cycle and two prominent classes of ubiquitin ligases, the SCF- and APC/C complexes. These ubiquitin ligases are reviewed with regard to their function in activating, maintaining, and terminating the checkpoint and in light of increasing evidence that suggests a dynamic balance of substrate ubiquitylation and deubiquitylation. We further discuss the impact of defective G2 checkpoint signaling on genomic stability and cancer risk, highlighting strategies for targeted antitumor drug discovery. [ABSTRACT FROM AUTHOR]

Background: The possible benefit of lifetime physical activity (PA) in reducing prostate cancer incidence and mortality is unclear.Methods: A prospective cohort of 45,887 men aged 45-79 years was followed up from January 1998 to December 2007 for prostate cancer incidence (n=2735) and to December 2006 for its subtypes and for fatal (n=190) prostate cancer.Results: We observed an inverse association between lifetime (average of age 30 and 50 years, and baseline age) total PA levels and prostate cancer risk. Multivariate-adjusted incidence in the top quartile of lifetime total PA decreased by 16% (95% confidence interval (CI)=2-27%) compared with that in the bottom quartile. We also observed an inverse association between average lifetime work or occupational activity and walking or bicycling duration and prostate cancer risk. Compared with men who mostly sit during their main work or occupation, men who sit half of the time experienced a 20% lower risk (95% CI=7-31%). The rate ratio linearly decreased by 7% (95% CI=1-12%) for total, 8% (95% CI=0-16%) for localised and 12% (95% CI=2-20%) for advanced prostate cancer for every 30 min per day increment of lifetime walking or bicycling in the range of 30 to 120 min per day.Conclusions: Our results suggest that not sitting for most of the time during work or occupational activity and walking or bicycling more than 30 min per day during adult life is associated with reduced incidence of prostate cancer. [ABSTRACT FROM AUTHOR]

The transcription factor p73, a member of the p53 family, mediates cell-cycle arrest and apoptosis in response to DNA damage-induced cellular stress, acting thus as a proapoptotic gene. Similar to p53, p73 activity is regulated by post-translational modification, including phosphorylation, acetylation and ubiquitylation. In C. elegans, the F-box protein FSN-1 controls germline apoptosis by regulating CEP-1, the single ancestral p53 family member. Here we report that FBXO45, the human ortholog of FSN-1, binds specifically to p73 triggering its proteasome-dependent degradation. Importantly, SCFFBXO45 ubiquitylates p73 both in vivo and in vitro. Moreover, siRNA-mediated depletion of FBXO45 stabilizes p73 and concomitantly induces cell death in a p53-independent manner. All together, these results show that the orphan F-box protein FBXO45 regulates the stability of p73, highlighting a conserved pathway evolved from nematode to human by which the p53 members are regulated by an SCF-dependent mechanism. [ABSTRACT FROM AUTHOR]

Cyclin A accumulates at the onset of S phase, remains high during G2 and early mitosis and is degraded at prometaphase. Here, we report that the acetyltransferase P/CAF directly interacts with cyclin A that as a consequence becomes acetylated at lysines 54, 68, 95 and 112. Maximal acetylation occurs simultaneously to ubiquitylation at mitosis, indicating importance of acetylation on cyclin A stability. This was further confirmed by the observation that the pseudoacetylated cyclin A mutant can be ubiquitylated whereas the nonacetylatable mutant cannot. The nonacetylatable mutant is more stable than cyclin A WT (cycA WT) and arrests cell cycle at mitosis. Moreover, in cells treated with histone deacetylase inhibitors cyclin A acetylation increases and its stability decreases, thus supporting the function of acetylation on cyclin A degradation. Although the nonacetylatable mutant cannot be ubiquitylated, it interacts with the proteins needed for its degradation (cdks, Cks, Cdc20, Cdh1 and APC/C). In fact, its association with cdks is increased and its complexes with these kinases display higher activity than control cycA WT–cdk complexes. All these results indicate that cyclin A acetylation at specific lysines is crucial for cyclin A stability and also has a function in the regulation of cycA-cdk activity.Oncogene (2009) 28, 2654–2666; doi:10.1038/onc.2009.127; published online 1 June 2009 [ABSTRACT FROM AUTHOR]

Increased concentrations of insulin, glucose and glycohemoglobin are associated with Type II diabetes mellitus (DM) and recognized as characteristic markers of the disease; in Alzheimer’s (AD), Vascular dementia (VaD), and both dementia’s with superimposed diabetes (AD + DM, VaD + DM) the knowledge is scarce. The sample ( n = 122; males = 60; mean age = 73 ± 7) comprised DM, AD, VaD, AD + DM, and VaD + DM patients, and healthy controls (C). The ANOVA’s yielded significant differences between groups: Insulin p = 3.7 × 10−3; Glucose p < 10−12; Glycohemoglobin p = 9.2×10−4. Comparisons between groups (DM vs. C, AD + DM vs. AD, VaD + DM vs. VaD, and demented DM vs. non-demented DM) resulted significant for all variables (Bonferroni’s statistic, α = 0.05). Diabetic and diabetic demented patients presented significant increases largely different from controls (0.01 < p < 0.001), unlike the non-significant changes in their non-diabetic counterparts; linear relationships were found across all groups. The correlation’s insulin/glucose and insulin/glycohemoglobin change to positive within demented groups, indicating a different performance of insulin in demented and non-demented subjects. [ABSTRACT FROM AUTHOR]

Brevibacterium spp. were considered apathogenic until a few reports of infections in immunocompromised patients were published. Herein, we present a case of a catheter-related septicemia with Brevibacterium casei in an immunocompetent patient receiving continuous iloprost infusion for pulmonary arterial hypertension and review the clinical presentation of this mainly emerging opportunistic pathogen. [ABSTRACT FROM AUTHOR]

Studies integration of N[sup2] fixing trees into stable agroforestry systems in the tropics because of their ability to produce high biomass nitrogen and phosphorous yields when symbiotically associated with rhizobia and mycorrhizal fungi. Tree selected for the experiment; Procedure adopted for the study; Impact of dual inoculation on the height and growth of the tree.

OBJECTIVE: We investigated the prevalence of overweight and obesity and their relationships with the main cardiovascular risk factors in the population of Ventimiglia di Sicilia, a rural village in Southern Italy characterized by low cholesterol levels and by a low incidence of early coronary heart disease mortality. We related all deaths to body weight and fat distribution during an 8 y follow-up. DESIGN: Cross-sectional and prospective observational study. SUBJECTS: A total of 835 free-living individuals, 363 males and 472 females, of age between 20 and 69 y. MEASUREMENTS: In all participants body weight, waist-to-hip ratio (WHR), cardiovascular risk factors and plasma lipids were measured. During the follow-up, total and cardiovascular deaths were registered. RESULTS: We found a high overall prevalence of subjects with overweight or obesity (respectively 45.0% and 27.7%), with great differences among classes of age. As expected, body weight and fat distribution were associated with diabetes, hypertension, dyslipidemia and with a worsening of lipid profile. During the follow-up we registered 37 total and 11 cardiovascular deaths. All-cause and cardiovascular mortality risks were, respectively, 1.64 (95% CI 0.65-4.15) and 2.71 (95% CI 0.29-25.26) in subjects with a body mass index (BMI) of 27-29.99 kg/m² and 2.45 (95% CI 1.03-5.87) and 5.36 (95% CI 1.41-62.01) in subjects with a BMI of ≥30kg/m² in comparison with participants with a BMI of <27 kg/m², and 3.48 (95% CI 1.46-8.30) and 4.55 (95% CI 1.12-18.40) in subjects with a WHR higher than the median in comparison with individuals with a WHR lower than the median. CONCLUSION: The Ventimiglia di Sicilia Study highlights the great importance of overweight and obesity as a public health issue in a rural population and indicates that it is necessary to consider the impact of body weight and fat distribution on both total and CHD mortality. [ABSTRACT FROM AUTHOR]

Ubiquitin-conjugation targets numerous cellular regulators for proteasome-mediated degradation. Thus, the identification of ubiquitin ligases and their physiological substrates is crucially important, especially for those cases in which aberrant levels of regulatory proteins (e.g., β-catenin, p27) result from a deregulated ubiquitination pathway. In yeast, the proteolysis of several G1 regulators is controlled by ubiquitin ligases (or SCFs) formed by three subunits: Skp1, Cul A (Cdc53), and one of many F-box proteins. Specific F-box proteins (Fbps) recruit different substrates to the SCF. Although many Fbps have been identified in mammals, their specific substrates and the existence of multiple SCFs have not yet been reported. We have found that one human Fbp, β-Trcp (β-Transducin repeat containing protein), does indeed form a novel SCF with human Skp1 and Cul1. Consistent with recent reports indicating that Xenopus and Drosophila β-Trcp homologs act as negative regulators of the Wnt/β-catenin signaling pathway, we report here that human β-Trcp interacts with β-catenin in vivo. Furthermore, β-catenin is specifically stabilized in vivo by the expression of a dominant negative β-Trcp. These results indicate that the Cul1/Skp1/β-Trcp complex forms a ubiquitin ligase that mediates the degradation of β-catenin. [ABSTRACT FROM AUTHOR]

Ubiquitin-mediated proteolysis is involved in the turnover of many short-lived regulatory proteins. This pathway leads to the covalent attachment of one or more multiubiquitin chains to target substrates which are then degraded by the 26S multicatalytic proteasome complex. Multiple classes of regulatory enzymes have been identified that mediate either ubiquitin conjugation or ubiquitin deconjugation from target substrates. Timed destruction of cellular regulators by the ubiquitin-proteasome pathway plays a critical role in ensuring normal cellular processes. This review provides multiple examples of key growth regulatory proteins whose levels are regulated by ubiquitin-mediated proteolysis. Pharmacological intervention which alters the half-lives of these cellular proteins may have wide therapeutic potential. Specifically, prevention of p53 ubiquitination (and subsequent degradation) in human papilloma virus positive tumors, and perhaps all tumors retaining wild-type p53 but lacking the retinoblastoma gene function, should lead to programmed cell death. Specific inhibitors of p27 and cyclin B ubiquitination are predicted to be potent antiproliferative agents. Inhibitors of IκB ubiquitination should prevent NFκB activation and may have utility in a variety of autoimmune and inflammatory conditions. Finally, we present a case for deubiquitination enzymes as novel, potential drug targets. [ABSTRACT FROM AUTHOR]

The cell cycle has been the object of extensive studies for the past years. A complex network of molecular interactions has been identified. In particular, a class of cell cycle inhibitory proteins has been identified but details of the molecular mechanism of their action have yet to be resolved. These inhibitors regulate the progression through G1 and the G1/S transition via the inhibition of the cyclin-dependent kinase (Cdk) activity. The potential function of these negative regulators as tumor suppressors provides new insights into the link between the cell cycle and oncogenesis. Kip1 is a potent inhibitor of Cdks. In quiescent cells Kip1 accumulates without an increase in mRNA or protein synthesis. We demonstrated that cell cycle regulation of Kip1 levels, both in normal and transformed human cells, occurs via the ubiquitin-proteasome pathway. In a crude in vitro system, Kip1 is ubiquitinated and degraded in an ATP dependent manner and inhibition or depletion of the proteasome blocks Kip1 degradation. Human Ubc2 and Ubc3, the homologs of yeast Rad6 and Cdc34 gene products respectively, are specifically involved in the ubiquitination of Kip1. Compared to proliferating cells, quiescent cells contain a far lower amount of Kip1 ubiquitinating activity. These results represent the first demonstration that the ubiquitin-proteasome pathway plays a role in the regulation of a cell cycle protein in human cells, namely the Cdk inhibitor Kip1. The specific proteolysis of Kip1 may be involved in the pathway of inactivation of Cdks. [ABSTRACT FROM AUTHOR]

The cell cycle has been the object of extensive studies for the past years. A complex network of molecular interactions has been identified. In particular, a class of cell cycle inhibitory proteins has been cloned and characterized but details of the molecular mechanism of their action have yet to be resolved. These inhibitors regulate the progression through G1 and the G1/S transition via the inhibition of the cyclin-dependent kinase (Cdk) activity. The potential function of these negative regulators as tumor suppressors provides new insights into the link between the cell cycle and oncogenesis. p27 is a potent inhibitor of Cdks. In quiescent cells p27 accumulates without an increase in mRNA or protein synthesis. Cell cycle regulation of p27 levels, both in normal and transformed human cells, occurs via the ubiquitin-proteasome pathway and, compared to proliferating cells, quiescent cells contain a far lower amount of p27 ubiquitinating activity. The specific proteolysis of p27 is probably involved in the pathway of activation of Cdks. p27 is a phosphoprotein and its phosphorylation is cell cycle regulated. Often phosphorylation is a signal for ubiquitination. p27 is phosphorylated exclusively on serine by Erk1 and almost exclusively on threonine by Cdk1 in in vitro experiments. This finding raises the question of whether and how phosphorylation by these kinases is involved in the process of p27 proteolysis. [ABSTRACT FROM AUTHOR]

The reproduction of Eurytemora velox, a brackish copepod from temporary lakes of the south of France, was studied in winter and spring 1978, under various temperature and salinity conditions, using Chlorella sp. and Amphidinium sp. as food. Maximum numbers of successive eggs sacs (9), eggs per sac (39.3) and total egg production per female (311) were recorded for the witner generation, only 4.8, 34.8 and 109, respectively, for the spring generation. In contrast, the number of eggs per female per day was highest (11.3) in the spring generation, which displayed a more rapid reproductive cycle. Despite strong individual variations in the rhythm of egg sac production and in abundance of eggs per sac, egg production was generally higher during the first third of adult life, attaining a maximum after production of the second or the third egg sac. The continuous presence of the males was necessary to assure complete fertilization of eggs throughout the whole life of adult females. Hatching rate displayed high individual variability, in particular for the spring generation, which had lower average hatching rates (between 0 and 26%, depending on salinity or temperature) than the winter generation (14 to 64%). These differences may be related to the ability of E. velox to produce resting eggs during spring, allowing the species to maintain itself in a temporary water milieu. Temperature significantly affected longevity and daily egg production of females; presence or absence of males did not affect these parameters. An increase in salinity from 20 to 30%. reduced longevity, number of egg sacs, and daily egg production in the winter generation, but not in the spring generation. The specific daily production of females during their adult life was calculated from the egg production:biomass ratio of females, in carbon units. In the winter generation, this ratio increased between 10° and 15°C compared to ratios between 15° and 20°C; the opposite was observed for the spring generation. The seasonal differences in the effects of temperature and salinity on reproduction could indicate an adaptation mechanism to the strongly thermal and haline seasonal fluctuations which characterize the habitat of Ex. velox (brackish waters, drying-up in summer). Larval mortality was high, except at 20%. S for the spring generation. The sex-ratio of the offspring was unaffected by variations in breeding conditions. Hatching time and development time of larvae could be described by two Bělehrádek equations displaying close b and (α) coefficients. We calculated the energy balance of adult females from data obtained in a previous study on feeding and respiration in E. velox, and this is discussed in context with the egg production results. Net growth efficiency varied with algal concentration according to an asymptotic curve, reaching a maximum of 0.43 with Tetraselmis maculata as food or 0.53 with Amphidinium sp. Actual egg production rate obtained in the present study was in good agreement with that calculated by the difference between assimilated food and respiration expenses. [ABSTRACT FROM AUTHOR]

The respiration and excretion (ammonia and phosphate) of Eurytemora velox, a brackish copepod from temporary lakes of the south of France, were studied in 1978-1979 in relation to food ingestion, temperature and salinity. Suspensions of Tetraselmis maculata were used as food. Respiration was closely dependent on the quantity of the ingested food, displaying a linear relationship with a strong positive-slope coefficient. In most cases, the temperature effect on respiration and excretion was well described by a power-type equation ( M=a b, where M=metabolism and T=temperature) over a rather large temperature range. In some experiments, metabolism curves displayed a maximum at 20°C. The metabolismtem-temperature curves differed between successive experiments, depending on season and/or sampling area, perhaps as a result of different acclimatization processes developing in individuals from different generations and/or among geographically isolated populations. Salinity variations significantly affected respiration, but not excretion. Respiration increased in individuals placed in hypo- or hyper-salinity conditions for a period of 24 h. This inability for complete metabolic regulation is unexpected in a species from a habitat subjected to variable salinity, and may have resulted from a too short acclimatization time in the experiments. [ABSTRACT FROM AUTHOR]

Photon emitted in the visible and near ultraviolet range by germinating soya seeds has been measured by means of a low-noise photomultiplier coupled to a data acquisition system. The photon energy spectrum, determined by means of a set of optical filters, shows two main contributions in the red and UV bands. Results show that both the radiation intensity and its spectrum change during germination according to seed physiological conditions. The photon emission of seeds at rest changes with their germinability. The UV component at the germination beginning is a factor 6 larger for living seeds than for the devitalized ones. This result can be interpreted as an experimental evidence of the existence of mitogenetic radiation. [ABSTRACT FROM AUTHOR]