A comparative analysis for the volatile compounds of various Chinese dark teas using combinatory metabolomics and fungal solid-state fermentation

A total of 98 compounds including 20 aldehydes, eight arenes, six acids, 17 alcohols, 13 ketones, nine esters, nine methoxyphenolics, three alkenes, seven alkanes, and six other components were tentatively identified in six Chinese dark teas (CDTs) using gas chromatography–mass spectrometry. Multivariate statistical analysis revealed that dark teas from Yunnan and Guangxi provinces could be classified into one group, and other CDTs belonged to the other cluster. The diagnostic volatile compounds being responsible for CDTs' discrimination were observed as (E,E)-2,4-decadienal, methoxyphenolics, geraniol, α-terpineol, 2,4-heptadienal, cis-jasmone, linalool oxides, and 2-nonenal. Furthermore, mature tea leaves were separately fermented using Eurotium cristatum and Aspergillus niger. The results showed that E. cristatum increased the contents of cis-jasmone, α-terpineol, ß-ionone, nonanal, and 2-pentylfuran, whereas A. niger advanced the levels of geraniol, linalool oxides, 9,12-octadecadienoic acid, and ß-ionone after short-term fermentation. Fungus species may contribute to forming the flavor of Chinese dark teas by affecting the volatile compounds during postfermentation

Artificial neural network identified the significant genes to distinguish Idiopathic pulmonary fibrosis

Abstract Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease that causes irreversible damage to lung tissue characterized by excessive deposition of extracellular matrix (ECM) and remodeling of lung parenchyma. The current diagnosis of IPF is complex and usually completed by a multidisciplinary team including clinicians, radiologists and pathologists they work together and make decision for an effective treatment, it is imperative to introduce novel practical methods for IPF diagnosis. This study provided a new diagnostic model of idiopathic pulmonary fibrosis based on machine learning. Six genes including CDH3, DIO2, ADAMTS14, HS6ST2, IL13RA2, and IGFL2 were identified based on the differentially expressed genes in IPF patients compare to healthy subjects through a random forest classifier with the existing gene expression databases. An artificial neural network model was constructed for IPF diagnosis based these genes, and this model was validated by the distinctive public datasets with a satisfactory diagnostic accuracy. These six genes identified were significant correlated with lung function, and among them, CDH3 and DIO2 were further determined to be significantly associated with the survival. Putting together, artificial neural network model identified the significant genes to distinguish idiopathic pulmonary fibrosis from healthy people and it is potential for molecular diagnosis of IPF

The types of brewing water affect tea infusion flavor by changing the tea mineral dissolution

The effects of different brewing water samples, including natural drinking water (NDW), pure water (PW), mineral water (MW), distilled water (DW), and tap water (TW) on flavor and quality of green tea infusion were investigated. The results showed the dissolution rate of mineral substances varied greatly depend on the type of water used. Notably, the tea infusion brewed with MW showed the highest taste response and darker but higher brightness in color. Furthermore, the content of volatile compounds was highest in tea infusion brewed with NDW and lowest in tea infusion brewed with MW. The mineral substances content and pH were the main factors affecting volatile compounds in green tea infusion. Thereinto, Ca2+ and Fe3+ remarkably affected the content of alcohols and aldehydes in volatile compounds. These results suggested that water with a neutral pH value and lower mineral substance content is more conducive for brewing green tea

ADRB2 inhibition combined with antioxidant treatment alleviates lung fibrosis by attenuating TGFβ/SMAD signaling in lung fibroblasts

Abstract Idiopathic pulmonary fibrosis is a progressive and fatal interstitial lung disease with a poor prognosis and limited therapeutic options, which is characterized by aberrant myofibroblast activation and pathological remodeling of the extracellular matrix, while the mechanism remains elusive. In the present investigation, we observed a reduction in ADRB2 expression within both IPF and bleomycin-induced fibrotic lung samples, as well as in fibroblasts treated with TGF-β1. ADRB2 inhibition blunted bleomycin-induced lung fibrosis. Blockage of the ADRB2 suppressed proliferation, migration, and invasion and attenuated TGF-β1-induced fibroblast activation. Conversely, the enhancement of ADRB2 expression or functionality proved capable of inducing fibroblast-to-myofibroblast differentiation. Subsequent mechanistic investigation revealed that inhibition of ADRB2 suppressed the activation of SMAD2/3 in lung fibroblasts and increased phos-SMAD2/3 proteasome degradation, and vice versa. Finally, ADRB2 inhibition combined with antioxidants showed increased efficacy in the therapy of bleomycin-induced lung fibrosis. In short, these data indicate that ADRB2 is involved in lung fibroblast differentiation, and targeting ADRB2 could emerge as a promising and innovative therapeutic approach for pulmonary fibrosis

Fenbendazole Attenuates Bleomycin-Induced Pulmonary Fibrosis in Mice via Suppression of Fibroblast-to-Myofibroblast Differentiation

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, and fatal interstitial lung disease with unknown etiology. Despite substantial progress in understanding the pathogenesis of pulmonary fibrosis and drug development, there is still no cure for this devastating disease. Fenbendazole (FBZ) is a benzimidazole compound that is widely used as an anthelmintic agent and recent studies have expanded the scope of its pharmacological effects and application prospect. This study demonstrated that FBZ treatment blunted bleomycin-induced lung fibrosis in mice. In vitro studies showed that FBZ inhibited the proliferation and migration of human embryo lung fibroblasts. Further studies showed that FBZ significantly inhibited glucose consumption, moderated glycolytic metabolism in fibroblasts, thus activated adenosine monophosphate-activated protein kinase (AMPK), and reduced the activation of the mammalian target of rapamycin (mTOR) pathway, thereby inhibiting transforming growth factor-β (TGF-β1)-induced fibroblast-to-myofibroblast differentiation and collagen synthesis. In summary, our data suggested that FBZ has potential as a novel treatment for pulmonary fibrosis

Migration kinetics of four photo-initiators from paper food packaging to solid food simulants

<p>The migration behaviour of four photo-initiators (BP, EHA, MBP and Irgacure 907) was studied by ‘printing’ onto four different food-packaging materials (Kraft paper, white cardboard, Polyethylene (PE)-coated paper and composite paper) and tracking movement into the food simulant: Tenax-TA (porous polymer 2,6-diphenyl furan resin). The results indicated that the migration of the photo-initiators was related to the molecular weight and log <i>K</i>_o/w of each photo-initiator. At different temperatures, the migration rates of the photo-initiators were different in papers with different thicknesses. The amount of each photo-initiator found in the food was closely related to the food matrix. The Weibull model was used to predict the migration load into the food simulants by calculating the parameters <i>τ</i> and <i>β</i> and determining the relationship of the two parameters with temperature and paper thickness. The established Weibull model was then used to predict the migration of each photo-initiator with respect to different foods. A two-parameter Weibull model fitted the actual situation, with some deviation from the actual migration amount.</p

Tuftelin1 drives experimental pulmonary fibrosis progression by facilitating stress fiber assembly

Abstract Background Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease (ILD) with unknown etiology, characterized by sustained damage repair of epithelial cells and abnormal activation of fibroblasts, the underlying mechanism of the disease remains elusive. Methods To evaluate the role of Tuftelin1 (TUFT1) in IPF and elucidate its molecular mechanism. We investigated the level of TUFT1 in the IPF and bleomycin-induced mouse models and explored the influence of TUFT1 deficiency on pulmonary fibrosis. Additionally, we explored the effect of TUFT1 on the cytoskeleton and illustrated the relationship between stress fiber and pulmonary fibrosis. Results Our results demonstrated a significant upregulation of TUFT1 in IPF and the bleomycin (BLM)-induced fibrosis model. Disruption of TUFT1 exerted inhibitory effects on pulmonary fibrosis in both in vivo and in vitro. TUFT1 facilitated the assembly of microfilaments in A549 and MRC-5 cells, with a pronounced association between TUFT1 and Neuronal Wiskott-Aldrich syndrome protein (N-WASP) observed during microfilament formation. TUFT1 can promote the phosphorylation of tyrosine residue 256 (Y256) of the N-WASP (pY256N-WASP). Furthermore, TUFT1 promoted transforming growth factor-β1 (TGF-β1) induced fibroblast activation by increasing nuclear translocation of pY256N-WASP in fibroblasts, while wiskostatin (Wis), an N-WASP inhibitor, suppressed these processes. Conclusions Our findings suggested that TUFT1 plays a critical role in pulmonary fibrosis via its influence on stress fiber, and blockade of TUFT1 effectively reduces pro-fibrotic phenotypes. Pharmacological targeting of the TUFT1-N-WASP axis may represent a promising therapeutic approach for pulmonary fibrosis