Investigation of Cigarette Smoking among Male Schizophrenia Patients

Male schizophrenia patients are known to have a heavier smoking pattern compared with the general population. However, the mechanism for this association is not known, though hypothesis that smoking could alleviate symptomatology of schizophrenia and reduce side effects of antipsychotics has been suggested. The aims of this study were to validate the heavier smoking pattern among male schizophrenia patients and to investigate the possible mechanisms for the association. To enhance the reliability of the study, we recruited two large independent samples with 604 and 535 male Chinese schizophrenia patients, and compared their smoking pattern with that of 535 healthy male controls recruited from general population. Validated multiple indicators and multiple causes structure equation model and regression models were used to investigate the association of smoking with factors of schizophrenia symptomatology and with the usage of antipsychotics and their extra-pyramidal side effects (EPS). Schizophrenia patients had significantly heavier smoking pattern compared with healthy controls in our sample (42.4% vs. 16.8%, p<0.001 for current smoking prevalence; 23.5% vs. 43.3%, p<0.001 for smoking cessation rate; 24.5% vs. 3.0%, p<0.001 for heavy smoker proportion). Their smoking status was also found to be consistently and significantly associated with reduced negative factor scores for schizophrenia symptomatology (β = −0.123, p = 0.051 for sample-A; β = −0.103, p = 0.035 for sample-B; β = −0.082, p = 0.017 for the combined sample). However, no significant association was found between smoking and antipsychotics usage or risk of EPS. These results support that smoking is associated with improved negative symptoms, which could account for the heavier smoking pattern among schizophrenia patients.     

Solubilization of microsomal-associated phosphatidylserine synthase and phosphatidylinositol synthase from Saccharomyces cerevisiae

Membrane-associated cytidine 5'-diphospho-1,2-diacyl-sn-glycerol (CDP-diacylglycerol):L-serine O-phosphatidyltransferase (phosphatidylserine synthase, EC2.7.8.8.) and CDP-diacylglycerol:myo-inositol phosphatidyltransferase (phosphatidylinositol synthase, EC 2.7.8.11) were solubilized from the microsomal fraction of Saccharomyces cerevisiae. A variety of detergents were examined for their ability to release phosphatidylserine synthase and phosphatidylinositol synthase activities from the microsome fraction. Both enzymes were solubilized from the microsome fraction with Renex 690 in yield over 80% with increase to specific activity of 1.6-fold. Both solubilized enzymatic activities were dependent on manganese ions and Triton X-100 for maximum activity. The pH optimum for each reaction was 8.0. The apparent Km values for CDP-diacylglycerol and serine for the phosphatidylserine synthase reaction were 0.1 and 0.25 mM, respectively. The apparent Km values for CDP-diacylglycerol and inositol for the phosphatidylinositol synthase reaction were 70 microM and 0.1 mM, respectively. Thioreactive agents inhibited both enzymatic activities. Both solubilized enzymatic activities were thermally inactivated at temperatures above 30 degrees C.     

Refilling Nitrogen to Oxygen Vacancies in Ultrafine Tungsten Oxide Clusters for Superior Lithium Storage

Morphological engineering of nanosized transitional metal oxides shows great promise for performance improvement, yet limited efforts have been attempted to engineer the atomic structure. Oxygen vacancy (V_O) can boost charge transfer leading to enhanced performance; yet excessive V_O may impair the conductivity. Herein, tungsten oxide is atomically tailored by incorporating nitrogen heteroatoms into the oxygen vacancies. The efficient nitrogen‐filling into the oxygen vacancies is evidenced by the electron paramagnetic resonance spectroscopy and X‐ray absorption spectroscopy. The coordinated N atoms play a crucial role in facilitating the charge transfer and maintaining efficient lithium‐ion diffusion. Consequently, the tungsten oxide with N‐filled oxygen vacancies exhibits superior lithium‐ion storage performance.     

Life history traits and dispersal shape neutral genetic diversity in metapopulations

Journal of Mathematical Biology - In insect respiration, oxygen from the air diffuses through a branching system of air-filled tubes to the cells of the body and carbon dioxide produced in cellular...     

Early queen infection shapes developmental dynamics and induces long-term disease protection in incipient ant colonies

Infections early in life can have enduring effects on an organism's development and immunity. In this study, we show that this equally applies to developing ‘superorganisms’––incipient social insect colonies. When we exposed newly mated Lasius niger ant queens to a low pathogen dose, their colonies grew more slowly than controls before winter, but reached similar sizes afterwards. Independent of exposure, queen hibernation survival improved when the ratio of pupae to workers was small. Queens that reared fewer pupae before worker emergence exhibited lower pathogen levels, indicating that high brood rearing efforts interfere with the ability of the queen's immune system to suppress pathogen proliferation. Early-life queen pathogen exposure also improved the immunocompetence of her worker offspring, as demonstrated by challenging the workers to the same pathogen a year later. Transgenerational transfer of the queen's pathogen experience to her workforce can hence durably reduce the disease susceptibility of the whole superorganism.     

Dynamic Proteome Response of Pseudomonas aeruginosa to Tobramycin Antibiotic Treatment

Genetically susceptible bacteria become antibiotic tolerant during chronic infections, and the mechanisms responsible are poorly understood. One factor that may contribute to differential sensitivity in vitro and in vivo is differences in the time-dependent tobramycin concentration profile experienced by the bacteria. Here, we examine the proteome response induced by subinhibitory concentrations of tobramycin in Pseudomonas aeruginosa cells grown under planktonic conditions. These efforts revealed increased levels of heat shock proteins and proteases were present at higher dosage treatments (0.5 and 1 μg/ml), while less dramatic at 0.1 μg/ml dosage. In contrast, many metabolic enzymes were significantly induced by lower dosages (0.1 and 0.5 μg/ml) but not at 1 μg/ml dosage. Time course proteome analysis further revealed that the increase of heat shock proteins and proteases was most rapid from 15 min to 60 min, and the increased levels sustained till 6 h (last time point tested). Heat shock protein IbpA exhibited the greatest induction by tobramycin, up to 90-fold. Nevertheless, deletion of ibpA did not enhance sensitivity to tobramycin. It seemed possible that the absence of sensitization could be due to redundant functioning of IbpA with other proteins that protect cells from tobramycin. Indeed, inactivation of two heat shock chaperones/proteases in addition to ibpA in double mutants (ibpA/clpB, ibpA/PA0779 and ibpA/hslV) did increase tobramycin sensitivity. Collectively, these results demonstrate the time- and concentration-dependent nature of the P. aeruginosa proteome response to tobramycin and that proteome modulation and protein redundancy are protective mechanisms to help bacteria resist antibiotic treatments.The opportunistic pathogen Pseudomonas aeruginosa is ubiquitous in the natural environment and causes human infections (1). P. aeruginosa can metabolize various carbon and nitrogen compounds and persists under nutrient-poor and hostile growth environments (2, 3). One example is P. aeruginosa pulmonary infection of cystic fibrosis (CF) patients. Despite stress induced by host defenses and high concentrations of antibiotics, P. aeruginosa cells are able to persistently colonize CF airways (4).The aminoglycoside tobramycin is a front-line drug currently used in the treatment of P. aeruginosa in CF and other diseases. It is supplied in the forms of inhaled solution (TOBI) and intravenous injection. The tobramycin concentrations in airways after 300-mg dosage TOBI inhalation can reach 1,000 μg per g of sputum (5, 6). This concentration is in the range of 10 to 1,000 times of the minimal inhibitory concentration (MIC) for P. aeruginosa clinical isolates tested ex vivo (6). However, even with such high tobramycin concentrations, chronic P. aeruginosa infections are rarely eradicated (6). This is true even when the infecting bacteria are antibiotic sensitive, as is the case early in disease (7).One possible reason for P. aeruginosa persistence in vivo could relate to the time dependence of local concentrations of tobramycin experienced by P. aeruginosa in CF patient airways. Many factors, including inflammatory responses, blood and lymphatic circulations, and air flow distribution (for inhaled antibiotics), can alter the local antibiotic concentrations. In addition, P. aeruginosa cells can form biofilms in CF lungs and other infection sites (8), and biofilm exopolysaccharide layers may slow the diffusion of tobramycin (9, 10). P. aeruginosa cells in the inner layers of biofilms may experience lower concentrations and more gradual increase of tobramycin levels than those in outer layers (10, 11). Furthermore, even if final tobramycin concentration levels inside the biofilm eventually grow to match the highest levels experienced elsewhere, bacteria in these inner regions have experienced a slower increase, during which time proteome levels could be altered to promote the “adapted resistant state” (12). Adaptive resistance can also be induced in planktonic (free-living) P. aeruginosa (13, 14), and conventional MIC assays are not designed to measure this.Once induced, the adaptive resistance confers bacteria higher resistance to antibiotic treatments (13, 14) and is associated with decreased clinical antibiotic treatment efficacy (15). Interestingly, the adaptive resistance is time dependent and reversible. Typical adaptive resistance was observed starting 1 h after antibiotic exposure, and the drug susceptibility was regained after 36 h intervals (14, 15). Thus, adaptive resistance mechanisms may contribute in part to the disparity of in vivo persistence and ex vivo susceptibility to antibiotics in MIC tests.As an initial step toward defining adaptive resistance mechanisms, we investigated the time- and concentration-dependence of P. aeruginosa proteome response to tobramycin in planktonic conditions. Since the most effective protective responses may operate before killing begins and the rate of change of drug levels is likely to depend on ambient conditions, we studied bacteria exposed to low, subinhibitory levels of tobramycin (0.1, 0.5, and 1.0 μg/ml) at a range of time points (15, 60, 120, and 360 min) after exposure. The candidate proteome marker of P. aeruginosa for tobramycin response, heat shock protein IbpA, was further investigated with genetic mutagenesis and MIC assays.     

Characterizing Tropical Tree Species Growth Strategies: Learning from Inter-Individual Variability and Scale Invariance

Understanding how tropical tree species differ in their growth strategies is critical to predict forest dynamics and assess species coexistence. Although tree growth is highly variable in tropical forests, species maximum growth is often considered as a major axis synthesizing species strategies, with fast-growing pioneer and slow-growing shade tolerant species as emblematic representatives. We used a hierarchical linear mixed model and 21-years long tree diameter increment series in a monsoon forest of the Western Ghats, India, to characterize species growth strategies and question whether maximum growth summarizes these strategies. We quantified both species responses to biotic and abiotic factors and individual tree effects unexplained by these factors. Growth responses to competition and tree size appeared highly variable among species which led to reversals in performance ranking along those two gradients. However, species-specific responses largely overlapped due to large unexplained variability resulting mostly from inter-individual growth differences consistent over time. On average one-third of the variability captured by our model was explained by covariates. This emphasizes the high dimensionality of the tree growth process, i.e. the fact that trees differ in many dimensions (genetics, life history) influencing their growth response to environmental gradients, some being unmeasured or unmeasurable. In addition, intraspecific variability increased as a power function of species maximum growth partly as a result of higher absolute responses of fast-growing species to competition and tree size. However, covariates explained on average the same proportion of intraspecific variability for slow- and fast-growing species, which showed the same range of relative responses to competition and tree size. These results reflect a scale invariance of the growth process, underlining that slow- and fast-growing species exhibit the same range of growth strategies.