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The thiols, aldehyde and phenolic groups in EPS were responsible for selenite reduction. Under selenite stress, EPS was capable of increasing cell survivability by enhancing microorganisms-mediated selenite reduction. This work revealed the previously undiscovered roles of EPS in selenite reduction and elemental selenium formation in aquatic environments and also suggested a possible crucial role of EPS in selenium biogeochemical cycle. Most crime scene DNA evidence is retrieved using cotton swabs. Since the late 90's, the double-swab technique has been favoured by many practitioners throughout the world. However, the superiority of double-swabbing over applying single wet swabs has not been broadly verified. Here we set out to evaluate the need for the second dry swab for various surfaces, aiming at mimicking the range of surfaces encountered at crime scenes flat and ridged, absorbing and non-absorbing. For the tested non-absorbing surfaces, i.e., window glass, steel, brass, synthetic leather and ridged plastic, the first wet swabs gave at least 16 times higher DNA yields compared to the second dry swabs. In addition, second wet swabs gave more DNA than second dry ones, opposing the common notion that the purpose of the second swab is to absorb excess liquid. When ten experienced staff members sampled saliva stains on a window glass surface the variation between persons was considerable, with mean DNA yields for the first wet swabs ranging from 0.045 ± 0.022 to 0.13 ± 0.024 ng/μL. The first wet swabs gave 4-162 times more DNA than the second dry swabs, with higher DNA amounts on second swabs coinciding with lower amounts for first swabs. We show that for non-absorbing surfaces, the first wet swab takes up most of the cells in dried stains, making it less valuable to apply a second dry swab. The differences in DNA recovery between first and second swabs were notable also for absorbing surfaces. Double-swabbing may be preferable for some complex surfaces, but focusing on efficient sampling technique with single wet swabs is likely a better general approach. Paternity testing involving close relatives is facing challenges in the field of forensic genetics. Microhaplotype has been proposed as a promising genetic marker for their low mutation rates and high discrimination power recently. ULK-101 In this study, we selected 30 microhaplotypes from 1000 genome projects, including one non-binary SNP, and other six microhaplotypes from published studies containing only binary SNPs to established a panel of microhaplotypes for paternity testing. Most microhaplotypes generated a high effective number of alleles (Ae) with the harmonic mean value of Ae of 3.91 and the arithmetic mean value of heterozygosity of 0.74, respectively. We collected 54 unrelated individuals and 53 samples from six extended families. It was noting that 13 samples from six extended families were unrelated so they were also included in unrelated individuals. The pedigrees of 38 parent-child duos, 55 uncle/aunt/grandparent-child duos (non-biological parent-child duos) and 29 full sibling pairs were constructend microhaplotypes, all the non-biological parent-child duos could be considered as exclusions. The efficiency of excluding close relatives for this panel was evaluated by analyzing the parameters of 2000 simulated pairs, and the effectiveness was 0.988 at the threshold of t1 = 4 and t2 = -4. Moreover, the average Log10 combined full sibling index (CFSI) for all 29 full sibling pairs was about 7.55 after physical linkage taken account. These data demonstrated that this nonbinary SNPs-based microhaplotype panel has advantages in paternity testing, especially in STR mutated or close relatives involved cases. Myelosupression resulting from chemotherapy has been widely described in veterinary medicine; however, there is limited information relating to alterations in neutrophil function after chemotherapy in dogs with cancer. The aim of this study was to determine the non-proliferative effects of vincristine, carboplatin, and cisplatin on canine neutrophils by evaluating activation of oxidative and non-oxidative responses. Neutrophils were isolated from venous blood. Levels of reactive oxygen species (ROS) and metalloproteinase 9 (MMP-9) were measured in vitro during neutrophil exposure to these chemotherapeutic agents for 15 min followed by stimulation with platelet activating factor (PAF). ROS production was detected via luminescence, and MMP- 9 liberation was determined by zymography. The chemotherapeutic agents caused an increase in PAF-induced ROS production, but no change in the non-oxidative response was observed. These results suggest that these chemotherapeutic agents may act as priming agents by increasing the oxidative response. These effects could be beneficial for dogs with cancer by supporting their immune systems; however, excessive ROS liberation has been associated with inflammation, neutrophil-mediated cell injury, carcinogenesis, and metastasis. Clinical studies are necessary to evaluate the significance of these findings. Rapid and efficient speech processing benefits from the prediction derived from prior expectations based on the identification of individual words. It is known that speech processing is carried out within a distributed frontotemporal network. However, the spatiotemporal causal dynamics of predictive brain mechanisms in sound-to-meaning mapping within this network remain unclear. Using magnetoencephalography, we adopted a semantic anomaly paradigm which consists of expected, unexpected and time-reversed Mandarin Chinese speech, and localized the effects of violated expectation in frontotemporal brain regions, the sensorimotor cortex and the supramarginal gyrus from 250 ms relative to the target words. By further investigating the causal cortical dynamics, we provided the description of the causal dynamic network within the framework of the dual stream model, and highlighted the importance of the connections within the ventral pathway, the top-down modulation from the left inferior frontal gyrus and the cross-stream integration during the speech processing of violated expectation. INTRODUCTION During pregnancy, maternal stressors cause changes in both maternal and fetal HPA axes. We therefore investigated the impact of maternal non chronic and chronic stress on fetal glucose metabolism and growth, and serum levels of cortisol in the fetus. MATERIALS AND METHODS Normal weight pregnant women (n = 192; mean ± SD 27.9 ± 4.2 years old, and; 26.9 ± 2.4 kg/m²) were assessed during the 2nd and 3rd trimester with anthropometry, fetal ultrasound, blood samples for serum CRH, cortisol and IL6, and STAI trait and state stress questionnaires. We measured serum cortisol, insulin and c-peptide, and plasma glucose from cord blood. Neonates underwent anthropometry at the 3rd post-delivery day. RESULTS In both 2nd and 3rd trimesters, women with STAI trait scores ≥40 had significantly greater levels of fasting serum CRH and cortisol than those with STAI trait scores less then 40. 2nd trimester STAI trait scores correlated positively with cord blood glucose and c-peptide. Maternal serum CRH correlated negf both CRH and cortisol correlated positively with cord blood c-peptide, glucose, and insulin. STAI trait was the best positive predictor of cord blood cortisol, glucose and c-peptide, whilst STAI state was the best positive and negative predictor, respectively of fetal abdominal circumference and fetal head circumference or biparietal diameter. CONCLUSIONS Increased maternal chronic stress (reflected by the STAI trait score) associates with increased fetal cortisol, glucose, c-peptide secretion and thus, insulin resistance. Maternal non chronic stress (STAI state) in the 3rd trimester associates with changes in fetal growth pattern, including increased and decreased measurements of fetal abdominal and head growth respectively. Second generation antipsychotics, particularly olanzapine, induce severe obesity, which is associated with their antagonistic effect on the histamine H1 receptor (H1R). We have previously demonstrated that oral administration of olanzapine increases the concentration of neuropeptide Y (NPY) in the hypothalamus of rats, accompanied by hyperphagia and weight gain. However, it is unclear if the increased NPY after olanzapine administration is due to its direct effect on hypothalamic neurons and its H1R antagonistic property. In the present study, we showed that with an inverted U-shape dose-response curve, olanzapine increased NPY expression in the NPY-GFP hypothalamic neurons; however, this was not the case in the hypothalamic neurons of H1R knockout mice. Olanzapine inhibited the interaction of H1R and GHSR1a (ghrelin receptor) in the primary mouse hypothalamic neurons and NPY-GFP neurons examined by confocal fluorescence resonance energy transfer (FRET) technology. Furthermore, an H1R agonist, FMPH inhibited olanzapine activation of GHSR1a downstream signaling pAMPK and transcription factors of NPY (pFOXO1 and pCREB) in the hypothalamic NPY-GFP cell. However, an olanzapine analogue (E-Olan) with lower affinity to H1R presented negligible enhancement of pCREB within the nucleus of NPY neurons. These findings suggest that the H1R antagonist property of olanzapine inhibits the interaction of H1R and GHSR1a, activates GHSR1a downstream signaling pAMPK-FOXO1/pCREB and increases hypothalamic NPY this could be one of the important molecular mechanisms of H1R antagonism of olanzapine-induced obesity in antipsychotic management of psychiatric disorders. In this study, a series of thieno [2,3-d]pyrimidine derivatives were designed, synthesized and evaluated as novel AKT1 inhibitors. In vitro antitumor assay results showed that compounds 9d-g and 9i potently suppressed the enzymatic activities of AKT1 and potently inhibited the proliferation of HepG2, Hep3B, Huh-7 and SMMC-7721 cancer cell lines. Among these derivatives, the compound 9f demonstrated the best inhibitory activities on AKT1 (IC50 = 0.034 μM) and Huh-7 cell (IC50 = 0.076 μM). A panel of biological assays showed that compound 9f suppressed the cellular proliferation of Huh-7 through Akt/mTOR signaling pathway mediated autophagy mechanism. Furthermore, the antitumor capacity of 9f was validated in the subcutaneous Huh-7 xenograft models. Together, our results demonstrate that a novel small-molecule Akt1 inhibitor induces autophagy associated death in hepatocellular carcinoma, which may afford a potential drug candidate for targeted cancer therapy. Based on the definite therapeutic benefits, such as neuroprotective, cardioprotective, anticancer, anti-diabetic and so on, the Panax genus which contains many valuable plants, including ginseng (Panax ginseng C.A. Meyer), notoginseng (Panax notoginseng) and American ginseng (Panax quinquefolius L.), attracts research focus. Actually, the biological and pharmacological effects of the Panax genus are mainly attributed to the abundant ginsenosides. However, the low membrane permeability and the gastrointestinal tract influence seriously limit the absorption and bioavailability of ginsenosides. The acid or base hydrolysates of ginsenosides, 20 (R,S)-panaxadiol and 20 (R,S)-protopanaxadiol showed improved bioavailability and diverse pharmacological activities. Moreover, relative stable skeletons and active hydroxyl group at C-3 position and other reactive sites are suitable for structural modification to improve biological activities. In this review, the pharmacological activities of panaxadiol, protopanaxadiol and their structurally modified derivatives are comprehensively summarized.

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