Effect of Ag modification on TiO2 and melem/g-C3N4 composite on photocatalytic performances.

Here, the comparison of two different semiconductor materials is demonstrated, TiO2 and melem/g-C3N4 composites-modified with balls of approximately 5 nm Ag nanoparticles (NPs) as photocatalysts for the degradation of the model dye acid orange 7 (AO7). The melem molecule synthesized here is one of a series of organic compounds consisting of triazine ring compounds with a structure similar to that of melam and melamine. The photodegradation process of AO7 was carried out to examine all powder materials as a potential photocatalyst. Additionally, two different lamps of wavelengths 368 nm (UV light) and 420 nm (VIS light) were applied to compare the photodegradation tests. A new synthesis route for the acquisition of Ag NPs (Ag content 0.5, 1.0 and 2.5 wt%), based on a wet and low temperature method without the use of reducing reagents was proposed. The best photocatalytic performances under UV and VIS light were obtained for both, TiO2 and melem/g-C3N4 materials (new synthesis route) modified with a very low Ag content-0.5 wt%. The photodegradation activities using UV lamp (3 h, 368 nm irradiation) for samples with 0.5 wt% of Ag: TiO2 and melem/g-C3N4, in excess of 95 and 94%, respectively, were achieved. The highest photoactive materials melem/g-C3N4 with 0.5 and 1 wt% Ag revealed 98% of activity under the VIS lamp after 3 h long irradiation. Our work demonstrates a novel, environmentally acceptable, and cost-effective chemical strategy for preparation of photocatalysts suitable for degradation of organic contaminants in wastewater treatment.

SARS-CoV-2 genome quantification in wastewaters at regional and city scale allows precise monitoring of the whole outbreaks dynamics and variants spreading in the population.

SARS-CoV-2 is a coronavirus causing a globalized outbreak called COVID-19. SARS-CoV-2 transmission is associated with inhalation of contaminated respiratory droplets and could causes severe complications. Until today several "waves" of infections have been observed despite implementation of strict health policies. Decisions for such sanitary measures are based on population health monitoring. Unfortunately, for COVID-19, a significant proportion of individuals are asymptomatic but play a role in the virus transmission. To overcome these limitations, several strategies were developed including genome quantification in wastewater that could allow monitoring of the health status of population, since shedding of SARS-CoV-2 in patient stool is frequent. Wastewater-based epidemiology (WBE) was established and several countries implemented this approach to allow COVID-19 outbreak monitoring. In France, the OBEPINE project performed a quantitative analysis of SARS-CoV-2 in raw wastewater samples collected from major wastewater treatment plants (WWTP) since March 2020. In the greater Paris area 1101 samples (507 for five WWTP and 594 for sewer) were collected. This 16 months monitoring allows us to observe the outbreak dynamics. Comparison of WBE indicators with health data lead to several important observation; the good level of correlation with incidence rates, the average 3 days lead time, and the sensitivity (WBE change when incidence is > to 7/100000 inhabitants). We also compared the local monitoring (city level) with the regional monitoring, to help cluster identification. Moreover, variants of concern (VOC) emerged due to the selection pressure. We developed a specific RT-qPCR method targeting the deletion H69-V70 in the spike protein, using this deletion as a proxy of the B.1.1.7 presence in the wastewater. With this data we demonstrate the predominant role played by this strain in the third wave. All these results allow a better description and understanding of the pandemic and highlight the role of such WBE indicators.

Speciation and phylogeography of giant petrels Macronectes.

We examine global phylogeography of the two forms of giant petrel Macronectes spp. Although previously considered to be a single taxon, and despite debate over the status of some populations and the existence of minimal genetic data (one mitochondrial cytochrome b sequence per form), the current consensus based on morphology is that there are two species, Northern Giant Petrel M. halli and Southern Giant Petrel M. giganteus. This study examined genetic variation at cytochrome b as well as six microsatellite loci in giant petrels from 22 islands, representing most island groups at which the two species breed. Both markers support separate species status, although sequence divergence in cytochrome b was only 0.42% (corrected). Divergence was estimated to have occurred approximately 0.2mya, but with some colonies apparently separated for longer (up to 0.5 my). Three clades were found within giant petrels, which separated approximately 0.7mya, with the Southern Giant Petrel paraphyletic to a monophyletic Northern Giant Petrel. There was evidence of past fragmentation during the Pleistocene, with subsequent secondary contact within Southern Giant Petrels. The analysis also suggested a period of past population expansion that corresponded roughly to the timing of speciation and the separation of an ancestral giant petrel population from the fulmar Fulmarus clade.

Cocaine receptors on dopamine transporters are related to self-administration of cocaine.

Although cocaine binds to several sites in the brain, the biochemical receptor mechanism or mechanisms associated with its dependence producing properties are unknown. It is shown here that the potencies of cocaine-like drugs in self-administration studies correlate with their potencies in inhibiting [3H]mazindol binding to the dopamine transporters in the rat striatum, but not with their potencies in binding to a large number of other presynaptic and postsynaptic binding sites. Thus, the cocaine receptor related to substance abuse is proposed to be the one associated with dopamine uptake inhibition.

Determination of rpoA as the most suitable internal control to study stress response in C. jejuni by RT-qPCR and application to oxidative stress.

Campylobacter jejuni represents one of the major causes of bacterial enteritis caused by food in humans. There are still mechanisms to be deciphered to better understand better its physiology and pathogenesis. Study of gene expression levels by RT-qPCR could be used, but to be accurate and reproducible, a good internal control has to be chosen. The aim of this study was to identify a highly stable housekeeping gene in Campylobacter jejuni that could constitute a good internal control to study gene expression variations between different growth phases or stress conditions. Expression levels of six different housekeeping genes (gyrA, ilvC, rpoA, slyD, thiC and rrs) were measured by RT-qPCR under different conditions (exponential phase, stationary phase, cold shock, cold shock+oxidative stress, oxidative stress). The rpoA gene was chosen as the best internal control. In a previous study, 9 proteins were identified as involved in oxidative stress response, among which 3 virulence factors. Expression levels of genes coding for these proteins was evaluated by RT-qPCR using rpoA as an internal control. The results obtained were concordant with what had been observed at the proteomic level, validating the methods used and confirming the hypothesis of a potential link between oxidative stress and virulence factors expression.

Impacts of treatment parameters on the inactivation of Campylobacter jejuni by high pressure: a statistical study of main effects and interactions.

AIM: The influence of environmental (temperature and pH) and biological (strain) parameters on the inactivation of Campylobacter jejuni by high hydrostatic pressure (HHP) was investigated. METHODS AND RESULTS: Two clinical strains harvested in stationary phase were pressurized at 20 degrees C and 37 degrees C within a range of 50-400 MPa, in a phosphate (pH 7.0) or a citrate phosphate buffer (pH 5.6), for 10 min. Treatment efficiencies were determined by logarithmic comparisons of culturable cells on blood agar before and after treatment. Results were statistically compared using an anova of culturable cells after treatment to evaluate the effect of all factors. At least a 7-log reduction in cell numbers was observed for both strains. The pH and the strains had no effect on HHP treatment at 20 degrees C while at 37 degrees C, both pH and strain influenced significantly the HHP treatment on C. jejuni. CONCLUSIONS: The pressure efficacy on C. jejuni eradication was affected by both environmental and biological factors. SIGNIFICANCE AND IMPACT OF THE STUDY: Depending on the treatment conditions, C. jejuni sensitivity to HHP can significantly vary. The determination of the inactivation treatment by HPP has to be normalized considering the interaction of environmental and biological factors.

Effects of high pressure, subzero temperature, and pH on survival of Listeria monocytogenes in buffer and smoked salmon.

High pressure processing is a novel food preservation technology, applied for over 15 years in the food industry to inactivate spoilage and pathogenic microorganisms. Many studies have shown the differential resistance of bacterial cells to high pressure. Listeria monocytogenes is a bacterium able to grow at refrigerated temperature and to survive for a long time in minimally processed foods such as raw smoked fish. The freezing process does not cause significant decline of L. monocytogenes. The phase diagram of water under pressure permits a pressure treatment under subzero temperature, without the disadvantages of freezing for food quality. The aim of this study was to estimate if combined effects of pressure and subzero temperature could increase the destruction of L. monocytogenes in buffer and in smoked salmon. We investigated effects of high pressure processing (100, 150, and 200 MPa) combined with subzero temperatures (-10, -14, and -18 degrees C) and pH (7.0 and 4.5). Results showed that the most effective high-pressure treatment to inactivate L. monocytogenes was 200 MPa, -18 degrees C, and pH 4.5. The relevance of pressure holding time and the synergistic effect of pressure coupled with the subzero temperature to inactivate bacteria are highlighted. Modifications of physical properties (color and texture) were a lightening of color and an increase of toughness, which might be accepted by consumers, since safety is increased.

JAM-A as a prognostic factor and new therapeutic target in multiple myeloma.

Cell adhesion in the multiple myeloma (MM) microenvironment has been recognized as a major mechanism of MM cell survival and the development of drug resistance. Here we addressed the hypothesis that the protein junctional adhesion molecule-A (JAM-A) may represent a novel target and a clinical biomarker in MM. We evaluated JAM-A expression in MM cell lines and in 147 MM patient bone marrow aspirates and biopsies at different disease stages. Elevated JAM-A levels in patient-derived plasma cells were correlated with poor prognosis. Moreover, circulating soluble JAM-A (sJAM-A) levels were significantly increased in MM patients as compared with controls. Notably, in vitro JAM-A inhibition impaired MM migration, colony formation, chemotaxis, proliferation and viability. In vivo treatment with an anti-JAM-A monoclonal antibody (αJAM-A moAb) impaired tumor progression in a murine xenograft MM model. These results demonstrate that therapeutic targeting of JAM-A has the potential to prevent MM progression, and lead us to propose JAM-A as a biomarker in MM, and sJAM-A as a serum-based marker for clinical stratification.

The dopamine hypothesis of the reinforcing properties of cocaine.

A variety of evidence suggests a 'dopamine hypothesis' for the reinforcing properties of cocaine. This hypothesis proposes that cocaine binds at the dopamine transporter and mainly inhibits neurotransmitter re-uptake; the resulting potentiation of dopaminergic neurotransmission in mesolimbocortical pathways ultimately causes reinforcement. This model suggests potential medications for treatment of cocaine abuse and dependence. Some, but not all, pharmacological data in humans support the hypothesis and additional experimentation is needed.

Influence of kinetic parameters of high pressure processing on bacterial inactivation in a buffer system.

High pressure processing is recently applied in the food industry to inactivate spoilage and pathogenic microorganisms. Bacterial cells exhibit various barosensibility, and the role of pressurization, depressurization and constant pressure stage remain unknown. We investigated the effect of high pressure processing on Salmonella typhimurium and Listeria monocytogenes cells at 400 and 500 MPa respectively in buffer pH 7 at 20 degrees C. We applied various pressurization/depressurization kinetic rates (1, 5 and 10 MPa/s for pressurization and 250, 20 and 5 MPa/s for depressurization), and various pulse series or pressure holding times. Results show that high pressure pulses reduced linearly the number of bacterial cells according to the product of pressure and time: we defined this product as a Barometric Power (BP). Reduction of both microorganisms increased when holding time increased from 5 to 20 min, and better results were obtained when the rate of pressurization and depressurization were increased.

Impaired gene transcription and nuclear protein kinase C activation in the brain and liver of aged rats.

The expression of the hsp70 and c-fos genes and the activation of nuclear protein kinase C (PKC) were studied in young and aged whole rats under heat-shock conditions. The induction of hsp70 and c-fos genes by heat shock were decreased several fold in the brain as well as in the liver of senescent animals. Nuclear run-off transcription assay indicated that this age-related impairment could be attributed to a block at the level of transcription. Nuclear PKC activation by heat shock was not apparent in old animals. Nuclear PKC involvement in the repression of transcription during senescence is postulated.

Psychostimulant drugs and a dopamine hypothesis regarding addiction: update on recent research.

Evidence that psychostimulant drugs interact principally with monoamines, and in particular with the mesolimbic pathway that utilizes dopamine as the neurotransmitter, has prompted the dopamine hypothesis of psychostimulant addiction. This hypothesis proposes that enhancement of dopamine neurotransmission in the mesolimbic pathway is fundamental to the reinforcing properties of many drugs of abuse. Cocaine, the best characterized psychostimulant, is seen to fulfil this hypothesis by blocking dopamine transporters, thereby preventing re-uptake of the neurotransmitter and enhancing its synaptic concentration (Fig. 1). This biochemical mechanism is supported by behavioural data. For example, concordance between binding to the transporter and changes in locomotor activity has been demonstrated for a large series of cocaine analogues. The dopamine hypothesis suggests possible pharmacotherapeutic strategies to combat psychostimulant use, and these approaches, including available human data and future directions of pharmacological treatments are discussed in this paper. The limitations of the dopamine hypothesis with respect to psychostimulant dependence and abuse liability are also summarized, to provide a broad perspective of the current status of this hypothesis.

Buspirone enhances benzodiazepine receptor binding in vivo.

The effects of buspirone on benzodiazepine receptors labelled in vivo with [3H]Ro 15-1788 were investigated. While buspirone did not affect the binding of benzodiazepine receptors in vitro, significant dose-related increases were observed in the in vivo labelling of benzodiazepine receptors in mice. However, similar results were also obtained with various neuroleptic agents and apomorphine. Potential mechanisms that may account for these results are discussed, but the data suggest caution in the use of [11C]Ro 15-1788 in positron emission tomography scanning in humans, since labelling by Ro 15-1788 may be affected by factors unrelated to direct changes at the benzodiazepine receptor site.

Characterisation of autoantibodies to peripheral myelin protein 22 in patients with hereditary and acquired neuropathies.

To investigate the possibility that an autoimmune mechanism may play a role in the hereditary neuropathy Charcot-Marie-Tooth type 1A (CMT1A), sera were analysed by Western blot for anti-peripheral myelin protein 22 (PMP22) autoantibodies. These sera were compared with sera from patients with CMT type 2 (CMT2), acquired peripheral neuropathies such as chronic inflammatory demyelinating neuropathy (CIDP), anti-MAG IgM neuropathy, Miller-Fisher syndrome (MFS), diabetic neuropathy and with control blood donors. Anti-PMP22 positive sera were detected in 70% of patients with CMT1 and unexpectedly in 60% of patients with CMT2. Interestingly, 44% of the patients with other peripheral neuropathies and 23% of the apparently healthy controls showed also anti-PMP22 antibody reactivity. Immunohistochemical analysis of the human anti-PMP22 antisera on healthy sural nerve sections and on PMP22-expressing COS cells revealed that these sera did not recognise endogenous PMP22. Our results indicate that anti-PMP22 autoantibodies are found in sera of patients with different types of peripheral neuropathies, but their role in the pathogenesis of these diseases remains to be determined.

Cocaine produces locomotor stimulation in SS but not LS mice: relationship to dopaminergic function.

Cocaine produces several behavioral effects, most notably locomotor stimulation. While low doses of cocaine have been shown to decrease locomotor activity, moderate to high doses in the range of 5-50 mg/kg usually produce a marked increase in locomotor activity in rodents. This study examined the effects of a range of cocaine doses, 1-75 mg/kg, on locomotor activity in LS/Ibg (LS) and SS/Ibg (SS) mice. At the lowest doses, activity was depressed in both lines, but to a greater extent in LS mice. As the dose of cocaine was increased, activity returned to baseline, and at the highest doses, increases in locomotor activity were found, but only in SS mice. In LS mice, cocaine was ineffective in increasing locomotor activity at any of the doses tested. Since striatal dopaminergic neurons influence locomotor activity, we also assessed ligand affinity and receptor density of dopamine transporters and dopaminergic D1 and D2 receptors in striatal tissue obtained from these two selected lines. No differences in these receptor binding parameters were found. However, because of their anomalous locomotor response to cocaine, LS mice may prove to be a valuable tool in increasing our understanding of those sites which mediate specific effects of cocaine.

Cocaine-induced convulsions: pharmacological antagonism at serotonergic, muscarinic and sigma receptors.

The concurrent influence of multiple neurotransmitter systems in mediating cocaine-induced convulsions is predicted by the results of previous receptor binding studies. The present results demonstrate that pharmacological manipulations of these predicted neurotransmitter systems alters the occurrence of cocaine-induced convulsions. The 5-HT reuptake inhibitor fluoxetine enhanced the occurrence and severity of convulsions produced by 100 mg/kg (-) cocaine, while the 5-HT2 receptor antagonists cinanserin, ketanserin and pirenperone antagonized cocaine-induced convulsions in a dose-dependent manner. Further, the M1 receptor antagonist pirenzepine antagonized cocaine-induced convulsions, but atropine did not. In addition, both the (+) and (-) stereoisomers of the sigma ligand SKF 10047 significantly attenuated cocaine-induced convulsions. (+)SKF 10047 was more potent than (-)SKF 10047 in this effect, suggesting a stereoselective effect at sigma receptor sites. In constrast, DA and NE neurotransmission do not appear to modulate the proconvulsant effects of cocaine in a specific, dose-dependent manner. Thus, of the CNS binding sites with which cocaine is known to interact, the results are consistent with the conclusion that 5-HT transporters and 5-HT2 receptor sites appear to be direct and primary sites related to cocaine-induced convulsions, while M1 and sigma binding sites appear to play important but secondary and modulatory roles in this response.

Cocaine toxicity: concurrent influence of dopaminergic, muscarinic and sigma receptors in mediating cocaine-induced lethality.

The concurrent influence of dopaminergic, sigma and muscarinic neurotransmitter systems in mediating cocaine-induced lethality is predicted by previous receptor binding results from our laboratories. The present results demonstrate that pharmacological manipulations of these predicted neurotransmitter systems alter the occurrence of cocaine-induced lethality in C57BL/6J mice. The dopamine reuptake inhibitor bupropion increased the number of occurrences of lethality produced by (-) cocaine, while the dopaminergic D1 antagonist SCH 23390, the muscarinic M1 antagonist pirenzepine, and the sigma ligand (+) SKF 10047 all significantly, but only partially, antagonized (-) cocaine-induced lethality. In addition, the protective effects against lethality of the drug combinations SCH 23390 + pirenzepine or SCH 23390 + SKF 10047 were greater than any of these drugs used alone. These results are consistent with those from the previous receptor binding studies, and provide converging supportive evidence that the lethal effects of cocaine depend upon concurrent interactions with dopaminergic, muscarinic M1 and sigma receptor sites.

Spermine interacts with cocaine binding sites on dopamine transporters.

These studies were designed to assess the potential interaction of the polyamine spermine with cocaine binding to dopamine and serotonin transporters. The results of the experiments presented here indicate that spermine inhibits binding of the cocaine congener [3H] CFT to striatal synaptosomal membranes. Further, although [3H] CFT is known to interact with both dopamine and serotonin transporters, our results indicate that the observed inhibition of [3H] CFT binding is likely to reflect a specific inhibition of binding to dopamine transporters. Spermine significantly inhibited the binding of both [3H] CFT and [3H] mazindol to dopamine transporters, while it had no apparent effects on the binding of the potent serotonin uptake inhibitor [3H] paroxetine. Finally, saturation experiments show that the inhibition of ligand binding to the cocaine binding site on dopamine transporters appears not to be due to a modification of ligand affinity for the transporter, but to a decrease in the apparent density of ligand binding sites. The results of these experiments indicate that endogenously produced polyamines can alter cocaine binding to the dopamine transporter. The results are discussed in terms of possible impact on novel approaches for pharmacologically manipulating cocaine reinforcement and craving in clinical treatments for cocaine addiction, as well as for emergency treatment of cocaine overdose.

Indomethacin antagonism of ethanol-induced sleep time: sex and genotypic factors.

Pretreatment with prostaglandin synthetase inhibitors (PGSI) significantly decreases the CNS effects of ethanol across the entire ethanol dose-response curve. PGSIs do not significantly affect ethanol metabolism. These effects have been shown in HS/Ibg, LS/Ibg, and SS/Ibg males and females. These strains of mice are useful in alcohol research but are not widely available. The present study examined the possibility of similar effects in C57BL/6 and C3H/2 mice of both sexes. PGSI pretreatment significantly reduced ethanol sleep time across both sexes and genotypes in a dose-dependent manner. Females of both strains required more PGSI to antagonize ethanol's actions relative to males. Within sex, mice with greater sensitivity to ethanol required more PGSI to optimally reduce sleep time than less sensitive mice. These results extend previous findings, and support our hypothesis that one of ethanol's primary mechanisms of action in the CNS is to increase the synthesis of prostaglandins.

Inbred rat strain comparisons indicate different sites of action for cocaine and amphetamine locomotor stimulant effects.

Cocaine and amphetamine produce several behavioral effects, most notably locomotor stimulation. Biochemically, evidence suggests specific involvement of dopaminergic systems, although not necessarily identical sites, in mediating cocaine- and amphetamine-induced locomotor stimulation. This study examined the effects of cocaine or amphetamine on locomotor activity in rats from the ACI, F344, LEW and NBR inbred strains. Dose-dependent increases in locomotor activity were found for both drugs in all strains. However, large potency and efficacy differences were found. Further, significant strain by drug interactions were found, in that the strain rank order for stimulant response to the two drugs was not identical. Since striatal dopaminergic neurons influence locomotor activity, we also assessed ligand affinity and receptor density of dopamine transporters and dopaminergic D1 and D2 receptors in striatal tissue from these same strains of rats. No differences in these receptor binding parameters were found. These findings support the conclusion that these two drugs produce their locomotor stimulant effects through different sites of action, and that genetic differences in response to these drugs at the behavioral level do not appear to be mediated significantly by differences in structure or number of striatal dopaminergic sites. The further use of genetic methods, however, may aid in determining the specific sites of action of these widely used stimulant drugs.