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•Propylene was successfully oxidized by an in situ electrosynthetic H2O2 oxidant medium under mild conditions.•Tandem oxidation of propylene to propene glycol by combining oxygen ...reduction with thermal oxidation of propylene.•Electron transfer and mass transport are balanced by optimizing the ratio of carbon-based ORR catalyst and TS-1.•Propylene was oxidized to propylene glycol efficiently, with high selectivity (79.7 %) and yield (4.28 mmol gcat-1h−1).
It is highly desirable to develop an efficient and sustainable strategy for converting propylene into high value-added products under mild conditions. In this work, the tandem oxidation of propylene to propylene glycol was achieved by coupling electrosynthesis of H2O2 by 2e- ORR on an oxygen-doped carbon catalyst with thermocatalytic oxidation of propylene by H2O2 on titanium silicalite-1 (TS-1) in a flow cell. For a composite catalyst with the optimal composition which balances electron transfer and H2O2 mass transport, the selectivity towards propylene glycol and the utilization efficiency of H2O2 can reach 79.7 % and 47.6 %, respectively. The yield of propylene glycol is 4.28 mmol gcat-1h−1. This study provides a promising approach to electrochemical propylene conversion in the future.
In this study, we aim to investigate the regulation of specific long non-coding RNAs (lncRNAs) on the progression of ischemia/reperfusion (I/R) injury. We identified and characterized the exosomes ...derived from mouse primary aortic endothelial cells. Subsequently, we found that these exosomes expressed typical exosomal markers and high levels of LINC00174, which significantly ameliorated I/R-induced myocardial damage and suppressed the apoptosis, vacuolation, and autophagy of myocardial cells. Mechanistic approaches revealed that LINC00174 directly interacted with SRSF1 to suppress the expression of p53, thus restraining the transcription of myocardin and repressing the activation of the Akt/AMPK pathway that was crucial for autophagy initiation in I/R-induced myocardial damage. Moreover, this molecular mechanism was verified by in vivo study. In summary, exosomal LINC00174 generated from vascular endothelial cells repressed p53-mediated autophagy and apoptosis to mitigate I/R-induced myocardial damage, suggesting that targeting LINC00174 may be a novel strategy to treat I/R-induced myocardial infarction.
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In the present study, Su and colleagues show that exosomal LINC00174 derived from vascular endothelial cells attenuates myocardial ischemia-reperfusion (I/R) injury by suppressing p53-mediated autophagy and apoptosis. This discovery reveals a new regulation mechanism for I/R-induced injury and provides a potential therapeutic strategy to treat I/R-induced myocardial infarction.
A G > C polymorphism (rs2910164) is located in the stem region opposite to the mature miR-146a sequence, which results in a change from G:U pair to C:U mismatch in the stem structure of miR-146a ...precursor. Here, we elucidated the biological significance of this polymorphism, based on cancer association study and cell model system. The cancer association study included 479 hepatocellular carcinoma (HCC) and 504 control subjects. We found that the genotype distribution of this polymorphism in HCC cases was significantly different from that in control subjects (P = 0.026). The association between the genotype and the risk of HCC was further analyzed using multivariate unconditional logistic regression, with adjustment for sex, age and hepatitis B virus status. The results revealed that male individuals with GG genotype were 2-fold more susceptible to HCC (odds ratio = 2.016, 95% confidence interval = 1.056–3.848, P = 0.034) compared with those with CC genotype. We next examined the influence of this polymorphism on the production of mature miR-146a and found that G-allelic miR-146a precursor displayed increased production of mature miR-146a compared with C-allelic one. Further investigations disclosed that miR-146a could obviously promote cell proliferation and colony formation in NIH/3T3, an immortalized but non-transformed cell line. These data suggest that the G > C polymorphism in miR-146a precursor may result in important phenotypic traits that have biomedical implications. Our findings warrant further investigations on the relation between microRNA polymorphism and human diseases.
Genomewide Association Study of Leprosy Zhang, Fu-Ren; Zhang, Chi; Zhang, Lin ...
The New England journal of medicine,
12/2009, Volume:
361, Issue:
27
Journal Article
Peer reviewed
Open access
Little is known about genetic susceptibility to infectious disease. This study implicates variation in genes encoding molecules in the NOD2 (nucleotide-binding oligomerization domain containing 2) ...signaling pathway (which regulates innate immunity) in susceptibility to infection with
Mycobacterium leprae
and leprosy.
This study implicates variation in genes encoding molecules in the NOD2 signaling pathway (which regulates innate immunity) in susceptibility to infection with
Mycobacterium leprae
and leprosy.
Leprosy is a chronic infectious disease caused by
Mycobacterium leprae
. It affects the skin and peripheral nerves and can cause irreversible impairment of nerve function and consequent chronic disabilities.
1
Despite a dramatic decrease in its prevalence over the past two decades (largely due to the worldwide introduction of multidrug therapy in 1982),
2
leprosy remains a major public health problem and one of the most important preventable disabilities in many developing countries.
3
It is therefore particularly unfortunate that research into the mechanisms underlying infection and clinical sequelae has been limited by the fact that
M. leprae
infects only humans and . . .
Chronic pain often leads to the development of sleep disturbances. However, the precise neural circuit mechanisms responsible for sleep disorders in chronic pain have remained largely unknown. Here, ...we present compelling evidence that hyperactivity of pyramidal neurons (PNs) in the anterior cingulate cortex (ACC) drives insomnia in a mouse model of nerve-injury-induced chronic pain. After nerve injury, ACC PNs displayed spontaneous hyperactivity selectively in periods of insomnia. We then show that ACC PNs were both necessary for developing chronic-pain-induced insomnia and sufficient to mimic sleep loss in naive mice. Importantly, combining optogenetics and electrophysiological recordings, we found that the ACC projection to the dorsal medial striatum (DMS) underlies chronic-pain-induced insomnia through enhanced activity and plasticity of ACC-DMS dopamine D1R neuron synapses. Our findings shed light on the pivotal role of ACC PNs in developing chronic-pain-induced sleep disorders.
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•ACC pyramidal neurons (PNs) are selectively activated during chronic-pain-induced insomnia•Lesion of ACC PNs abolishes chronic-pain-induced insomnia•Hyperactive ACC PNs control chronic-pain-induced insomnia via the DMS pathway•Enhanced plasticity of ACC PNs to DMS D1R-MSNs mediates insomnia
Over 50% of chronic pain patients experience insomnia. Li et al. reveal that heightened activity of anterior cingulate cortex excitatory neurons precisely governs chronic-pain-induced insomnia via the dorsal medial striatum pathway. This effect relies on enhanced plasticity in dopamine D1-receptor-positive medium spiny neurons.
In recent years, the sugarcane streak mosaic virus (SCSMV) has been the primary pathogen of sugarcane mosaic disease in southern China. In this study, the complete genome of a sugarcane mosaic sample ...(named YN-21) from Kaiyuan City, Yunnan Province, was amplified and sequenced. By comparing the amino acid sequences of YN-21 and 15 other SCSMV isolates from the NCBI database, the protease recognition site of SCSMV was determined. YN-21 had the highest nucleotide and amino acid identities of 97.66% and 99.30%, respectively, in comparison with the SCSMV isolate (JF488066). The P1 had the highest variability of 83.38–99.72% in the amino acid sequence, and 6K2 was the most conserved, with 97.92–100% amino acid sequence identity. A phylogenetic analysis of nucleotide and amino acid sequences clustered the 16 SCSMV isolates into two groups. All the Chinese isolates were clustered into the same group, and YN-21 was closely related to the Yunnan and Hainan isolates in China. Recombination analysis showed no major recombination sites in YN-21. Selective pressure analysis showed that the dN/dS values of 11 proteins of SCSMV were less than 1, all of which were undergoing negative selection. These results can provide practical guidance for monitoring SCSMV epidemics and genetics.
In this study, a large-scale serological survey of caprine arthritis encephalitis virus (CAEV) infection was conducted between March 2011 and October 2012. 3,437 goat blood or milk samples were ...collected from 65 goat farms throughout Taiwan. A commercial ELISA kit was used to detect antibodies against CAEV. The overall seropositive rate was 61.7% (2,120/3,437) in goats and in 98.5% (64/65) of goat farms. These results provide the first large-scale serological evidence for the presence of CAEV infection, indicating that the disease is widespread in Taiwan.
The Library of Integrated Network-based Cellular Signatures (LINCS) L1000 big data provide gene expression profiles induced by over 10 000 compounds, shRNAs, and kinase inhibitors using the L1000 ...platform. We developed csNMF, a systematic compound signature discovery pipeline covering from raw L1000 data processing to drug screening and mechanism generation. The csNMF pipeline demonstrated better performance than the original L1000 pipeline. The discovered compound signatures of breast cancer were consistent with the LINCS KINOMEscan data and were clinically relevant. The csNMF pipeline provided a novel and complete tool to expedite signature-based drug discovery leveraging the LINCS L1000 resources.
General anesthesia shares many similarities with natural sleep in behavior and electroencephalogram (EEG) patterns. The latest evidence suggests that general anesthesia and sleep-wake behavior may ...share overlapping neural substrates. The GABAergic neurons in the basal forebrain (BF) have recently been demonstrated to play a key role in controlling wakefulness. It was hypothesized that BF GABAergic neurons may participate in the regulation of general anesthesia. Here, using
fiber photometry, we found that the activity of BF GABAergic neurons was generally inhibited during isoflurane anesthesia, having obviously decreased during the induction of anesthesia and being gradually restored during the emergence from anesthesia, in Vgat-Cre mice of both sexes. Activation of BF GABAergic neurons with chemogenetic and optogenetic approaches decreased sensitivity to isoflurane, delayed induction, and accelerated emergence from isoflurane anesthesia. Optogenetic activation of BF GABAergic neurons decreased EEG δ power and the burst suppression ratio (BSR) during 0.8% and 1.4% isoflurane anesthesia, respectively. Similar to the effects of activating BF GABAergic cell bodies, photostimulation of BF GABAergic terminals in the thalamic reticular nucleus (TRN) also strongly promoted cortical activation and behavioral emergence from isoflurane anesthesia. Collectively, these results showed that the GABAergic BF is a key neural substrate for general anesthesia regulation that facilitates behavioral and cortical emergence from general anesthesia via the GABAergic BF-TRN pathway. Our findings may provide a new target for attenuating the depth of anesthesia and accelerating emergence from general anesthesia.
The basal forebrain (BF) is a key brain region controlling sleep-wake behavior. Activation of GABAergic neurons in the BF potently promotes behavioral arousal and cortical activity. Recently, many sleep-wake-related brain structures have been reported to participate in the regulation of general anesthesia. However, it is still unclear what role BF GABAergic neurons play in general anesthesia. In this study, we aim to reveal the role of BF GABAergic neurons in behavioral and cortical emergence from isoflurane anesthesia and elucidate the underlying neural pathways. Understanding the specific role of BF GABAergic neurons in isoflurane anesthesia would improve our understanding of the mechanisms of general anesthesia and may provide a new strategy for accelerating emergence from general anesthesia.
Defensive behavior, a group of responses that evolved due to threatening stimuli, is crucial for animal survival in the natural environment. For defensive measures to be timely and successful, a high ...arousal state and immediate sleep-to-wakefulness transition are required. Recently, the glutamatergic basal forebrain (BF) has been implicated in sleep-wake regulation; however, the associated physiological functions and underlying neural circuits remain unknown. Here, using in vivo fiber photometry, we found that BF glutamatergic neuron is activated by various threatening stimuli, including predator odor, looming threat, sound, and tail suspension. Optogenetic activation of BF glutamatergic neurons induced a series of context-dependent defensive behaviors in mice, including escape, fleeing, avoidance, and hiding. Similar to the effects of activated BF glutamatergic cell body, photoactivation of BF glutamatergic terminals in the ventral tegmental area (VTA) strongly drove defensive behaviors in mice. Using synchronous electroencephalogram (EEG)/electromyogram (EMG) recording, we showed that photoactivation of the glutamatergic BF-VTA pathway produced an immediate transition from sleep to wakefulness and significantly increased wakefulness. Collectively, our results clearly demonstrated that the glutamatergic BF is a key neural substrate involved in wakefulness and defensive behaviors, and encodes these behaviors through glutamatergic BF-VTA pathway. Overexcitation of the glutamatergic BF-VTA pathway may be implicated in clinical psychiatric diseases characterized by exaggerated defensive responses, such as autism spectrum disorders.
•Glutamatergic neurons in the BF responses to various threatening stimuli.•Optogenetic activation of BF glutamatergic neurons triggers a range of context-dependent defensive behaviors.•Activation of BF glutamatergic terminals in the VTA also strongly promotes defensive behavior.•Photoactivating glutamatergic BF-VTA pathway induces transition to wakefulness and increases amount of wakefulness.
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