Catalytic cracking of 1, 3, 5-triisopropylbenzene over silicoaluminophosphate with hierarchical pore structure

In order to prepare a highly active catalyst for the catalytic cracking of larger molecules, a novel micro-mesoporous silicoaluminophosphate composite (define as mesoporous SAPO-5) with hierarchical tri-modal pore size distributions has been firstly synthesized via post-synthetic method in acidic condition and subsequently characterized. Morphology control of the composite is attempted by adjusting pH value of the synthetic system. Three different morphologies of composite, including sphere-, rod- and net-like, are obtained in the different conditions. Possible mechanism for the formation of mesoporous SAPO-5 has been proposed. The mesoporous SAPO-5 exhibits higher cracking activity than conventional microporous SAPO-5 for cracking of 1, 3, 5-triisopropylbenzene (1, 3, 5-TIPB) under the same reaction conditions. The result indicates that the mesoporous SAPO-5 with hierarchical pore structure is favorable for catalytic cracking of large molecule. When the cumene as the reaction molecule, the microporous SAPO-5 catalyst exhibits higher conversion in catalytic cracking of cumene compared to the mesoporous SAPO-5, and the result may be attributed to that microporous SAPO-5 has much stronger acidity and specific selectivity than mesoporous SAPO-5 catalyst in catalytic cracking of cumene. Meanwhile, corresponding carbenium ion mechanism can account for the products formed during the whole reaction process

Vagal sensory neurons mediate the Bezold–Jarisch reflex and induce syncope

Abstract: Visceral sensory pathways mediate homeostatic reflexes, the dysfunction of which leads to many neurological disorders1. The Bezold–Jarisch reflex (BJR), first described2,3 in 1867, is a cardioinhibitory reflex that is speculated to be mediated by vagal sensory neurons (VSNs) that also triggers syncope. However, the molecular identity, anatomical organization, physiological characteristics and behavioural influence of cardiac VSNs remain mostly unknown. Here we leveraged single-cell RNA-sequencing data and HYBRiD tissue clearing4 to show that VSNs that express neuropeptide Y receptor Y2 (NPY2R) predominately connect the heart ventricular wall to the area postrema. Optogenetic activation of NPY2R VSNs elicits the classic triad of BJR responses—hypotension, bradycardia and suppressed respiration—and causes an animal to faint. Photostimulation during high-resolution echocardiography and laser Doppler flowmetry with behavioural observation revealed a range of phenotypes reflected in clinical syncope, including reduced cardiac output, cerebral hypoperfusion, pupil dilation and eye-roll. Large-scale Neuropixels brain recordings and machine-learning-based modelling showed that this manipulation causes the suppression of activity across a large distributed neuronal population that is not explained by changes in spontaneous behavioural movements. Additionally, bidirectional manipulation of the periventricular zone had a push–pull effect, with inhibition leading to longer syncope periods and activation inducing arousal. Finally, ablating NPY2R VSNs specifically abolished the BJR. Combined, these results demonstrate a genetically defined cardiac reflex that recapitulates characteristics of human syncope at physiological, behavioural and neural network levels

Tumor Cell “Slimming” Regulates Tumor Progression through PLCL1/UCP1‐Mediated Lipid Browning

Abstract Emerging evidence has highlighted the important role of abnormal lipid accumulation in cancer development and progression, but the mechanism for this phenomenon remains unclear. Here, it is demonstrated that phospholipase C‐like 1/uncoupling protein 1 (PLCL1)/(UCP1)‐mediated lipid browning promotes tumor cell “slimming” and represses tumor progression. By screening three independent lipid metabolism‐related gene sets in clear cell renal cell carcinoma (ccRCC) and analyzing the TCGA database, it is found that PLCL1 predicted a poor prognosis and was downregulated in ccRCC. Restoration of PLCL1 expression in ccRCC cells significantly represses tumor progression and reduces abnormal lipid accumulation. Additionally, a phenomenon called tumor cell “slimming,” in which tumor cell volume is reduced and lipid droplets are transformed into tiny pieces, is observed. Further studies show that PLCL1 promotes tumor cell “slimming” and represses tumor progression through UCP1‐mediated lipid browning, which consumes lipids without producing ATP energy. Mechanistic investigations demonstrate that PLCL1 improves the protein stability of UCP1 by influencing the level of protein ubiquitination. Collectively, the data indicate that lipid browning mediated by PLCL1/UCP1 promotes tumor cell “slimming” and consumes abnormal lipid accumulation, which represses the progression of ccRCC. Tumor cell “slimming” offers a promising new concept and treatment modality against tumor development and progression