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Liquid-liquid microextraction (LLME) combined with gas chromatography-mass spectrometry (GC-MS) and headspace-gas chromatography-ion mobility spectrometry (HS-GC-IMS) were used to detect the variations in volatile compounds during the distillation process of strong flavor raw Baijiu. The 3D fingerprint spectrum clearly showed a variation in volatile compounds from different distillation stages, and most alcohol-soluble and low molecular weight compounds showed a downward trend with the extension of distillation time, but water-soluble, high molecular weight and high boiling compounds showed the opposite result. Then, 50 aroma compounds were sniffed and identified by gas chromatography-olfactometry-mass spectrometry (GC-O-MS) and multivariate statistical analysis including principal component analysis (PCA) and partial least squares discriminant analysis (PLS-DA) confirmed four aroma active markers related to classification. Finally, the receiver operating characteristic (ROC) curve was further used to verify that ethyl butanoate and ethyl hexanoate were the most effective difference marker to distinguish the head Baijiu samples and butanoic acid was the most effective difference marker for distinguishing the heart Baijiu samples from the tail Baijiu samples. [Display omitted] • LLME coupled with GC-O-MS was used to analyze the changes of aroma active compounds. • GC-MS and GC-IMS were compared the differences in the detection of compounds. • ROC curve was used to verify the most effective difference markers. [ABSTRACT FROM AUTHOR]

Soy sauce aroma type baijiu (SSAB) is one of the four basic baijiu flavor types. It has an elegant sauce flavor, empty cup aroma, lasting, mellow and sweet entrance, soft with obvious acidity, delicate taste and long aftertaste. However, to date, no study has identified the key aroma compounds in SSAB. This study introduces SSAB and its production process, and summarizes the research status on flavor compounds. Through analysis and review, some assumptions are made to explain why the key aroma compound of SSAB remains unidentified. We provide insights for the analysis of key aroma compounds in SSAB and lay a theoretical foundation for the improvement and rapid development of SSAB quality. • Specific summarizes the research of key volatile compounds in soy sauce aroma type baijiu. • Summarizes the research of off-odor components in soy sauce aroma type baijiu. • First time to analyzes why the key flavor of soy sauce aroma type baijiu have not been discovered. [ABSTRACT FROM AUTHOR]

• The feruloyl esterase activity in different layers of Jiupei at different fermentation times were determined and tracked. • The microorganisms with feruloyl esterase activity were screened and identified in Jiupei of sesame-flavor baijiu. • The conditions of enzyme production were optimized by liquid fermentation. Baijiu is a national beverage in China. Some functional compounds have been identified in baijiu, one of which is ferulic acid. One route for in situ ferulic acid synthesis is catalysed by feruloyl esterase from microorganisms using baijiu raw materials as substrates. However, few studies have focused on microorganisms obtained from baijiu that have feruloyl esterase activity. In this work, microorganisms with feruloyl esterase activity were screened in the fermented raw materials of baijiu. Four different microorganisms with feruloyl esterase activity were identified, and one strain, designated J1, showed high feruloyl esterase activity. The strain J1 belonged to the genus Acetobacter and showed the closest relationship with Acetobacter fabarum and Acetobacter lovaniensis. The feruloyl esterase production capacity of J1 was confirmed, and the fermentation conditions were optimised. The optimal enzyme production conditions for the highest feruloyl esterase activity required an initial fermentation pH of 7.0 at 30 °C, an inoculation volume of 10 %, and culturing for 24 h. [ABSTRACT FROM AUTHOR]

The mechanisms initiating and perpetuating the fibrogenic response in the injured liver are not well understood. Hepatic stellate cells are activated by liver injury to become proliferative and fibrogenic myofibroblasts. Emerging evidence suggests that the sympathetic nervous system may play a role in the development of cirrhosis. It is not known, however, whether this requires a direct interaction between sympathetic neurotransmitters and stellate cell receptors, or results indirectly, from sympathetic effects on the vasculature. Using cultured hepatic stellate cells, we show that the sympathetic neurotransmitters, norepinephrine and neuropeptide Y, markedly stimulate the proliferation of activated, myofibroblastic, hepatic stellate cells. Norepinephrine, but not neuropeptide Y, also induces collagen gene expression. In conclusion, physiologically relevant concentrations of sympathetic neurotransmitters directly modulate the phenotype of hepatic stellate cells. This suggests that targeted interruption of sympathetic nervous system signaling in hepatic stellate cells may be useful in constraining the fibrogenic response to liver injury. [Copyright &y& Elsevier]

The mechanisms that initiate and perpetuate the fibrogenic response, during liver injury, are unclear. Animal studies, however, strongly support a role for the autonomic nervous system (ANS) in wound healing. Therefore, the ANS may also mediate the development of cirrhosis. Hepatic stellate cells (HSC), the liver’s major matrix-producing cells, are activated by injury to become proliferative, fibrogenic myofibroblasts. HSC respond to sympathetic neurotransmitters by changing phenotype, suggesting that HSC may be the cellular effectors of ANS signals that modulate hepatic fibrogenesis during recovery from liver damage. We show here that the parasympathetic neurotransmitter acetylcholine markedly stimulates the proliferation of myofibroblastic HSC and induces HSC collagen gene expression in these cells. By extending evidence that HSC are direct targets of the ANS, these results support the proposed neuroglial role of HSC in the liver and suggest that interrupting ANS signalling may be useful in constraining the fibrogenic response to liver injury. [Copyright &y& Elsevier]

[Display omitted] • Novel, potent and effective EZH2 degraders were developed. • Compound P4 can effectively induce EZH2 protein degradation and inhibit breast cancer cell growth. • Compound P4 can significantly decrease the degree of H3K27me3 in MDA-MB-231 cell line, induce apoptosis and G 0 /G 1 phase arrest in Pfeiffer and MDA-MB-231 cell lines. • Compound P4 significantly inhibited the migratory and invasive capacity of MDA-MB-231 cells at micromolar concentrations in a dose-dependent manner. • Adequate metabolic stability in vitro. EZH2 (enhancer of zeste homolog 2) is one of the most important histone methyltransferases (HMTs), and overexpression of EZH2 can lead to proliferation, migration and angiogenesis of tumor cells. But most of EZH2 inhibitors are only effective against some hematologic malignancies and have poor efficacy against solid tumors. Here, we report the design, synthesis, and evaluation of highly potent proteolysis targeting chimeric (PROTACs) small molecules targeting EZH2. We developed a potent and effective EZH2 degrader P4 , which effectively induced EZH2 protein degradation and inhibited breast cancer cell growth. Further studies showed that P4 can significantly decrease the degree of H3K27me3 in MDA-MB-231 cell line, induce apoptosis and G 0 /G 1 phase arrest in Pfeiffer and MDA-MB-231 cell lines. Therefore, P4 is a potential anticancer molecule for breast cancer treatment. [ABSTRACT FROM AUTHOR]

Leptin’s actions on certain cells require a leptin-inducible neurotransmitter, norepinephrine (NE). NE modulates hepatic fibrosis. Therefore, decreased NE may explain why leptin deficiency inhibits hepatic fibrosis. We manipulated adrenergic activity in leptin-deficient ob/ob mice, leptin-sufficient, dopamine β-hydroxylase deficient (Dbh−/−) mice, and HSC cultures to determine if leptin requires NE to activate HSC and induce hepatic fibrosis. ob/ob mice have chronic liver injury, but reduced numbers of HSC. Supplemental leptin increases HSC, suggesting that leptin-dependent, injury-related factors permit expansion of HSC populations. NE also increases HSC numbers and activation, normalizing fibrogenesis. When fed hepatotoxic diets, NE-deficient Dbh−/− mice fail to accumulate activated HSC and have impaired fibrogenesis unless treated with adrenergic agonists. NE acts directly on HSC to modulate leptin’s actions because leptin increases HSC proliferation and prazosin, an α-adrenoceptor antagonist, inhibits this. Thus, leptin permits injury-related increases in adrenergic activity and requires NE to activate HSC and induce hepatic fibrogenesis. [Copyright &y& Elsevier]