Explore the vast range of titles available.

Background Gallic acid has received a significant amount of interest for its biological properties. Thus, there have been recent attempts to apply this substance in various industries and in particular the feed industry. As opposed to yeasts, fungi and bacteria and their tannases have been well documented for their potential bioconversion and specifically for the biotransformation of tannic acid to gallic acid. In this research, Sporidiobolus ruineniae A45.2 is introduced as a newly pigment-producing and tannase-producing yeast that has gained great interest for its use as an additive in animal feed. However, there is a lack of information on the efficacy of gallic acid production from tannic acid and the relevant tannase properties. The objective of this research study is to optimize the medium composition and conditions for the co-production of gallic acid from tannic acid and tannase with a focus on developing an integrated production strategy for its application as a feed additive. Results Tannase produced by S. ruineniae A45.2 has been classified as a cell-associated tannase (CAT). Co-production of gallic acid obtained from tannic acid and CAT by S. ruineniae A45.2 was optimized using response surface methodology and then validated with the synthesis of 11.2 g/L gallic acid from 12.3 g/L tannic acid and the production of 31.1 mU/mL CAT after 48 h of cultivation in a 1-L stirred tank fermenter. Tannase was isolated from the cell wall, purified and characterized in comparison with its native form (CAT). The purified enzyme (PT) revealed the same range of pH and temperature optima (pH 7) as CAT but was distinctively less stable. Specifically, CAT was stable at up to 70 °C for 60 min, and active under its optimal conditions (40 °C) at up to 8 runs. Conclusion Co-production of gallic acid and CAT is considered an integrated and green production strategy. S. ruineniae biomass could be promoted as an alternative source of carotenoids and tannase. Thus, the biomass, in combination with gallic acid that was formed in the fermentation medium, could be directly used as a feed additive. On the other hand, gallic acid could be isolated and purified for food and pharmaceutical applications. This paper is the first of its kind to report that the CAT obtained from yeast can be resistant to high temperatures of up to 70 °C.

The COVID-19 outbreak has created a severe crisis for general economic situation. Despite the short time span of the pandemic, many innovations are implemented for organizational survival and recovery in the competitive market environment of digital age. This paper aims to find out significant factors and how they impact on E-commerce adoption of small and medium enterprises in Vietnam, especially in the epidemic time. The results reveal that technology perceived compatibility has the greatest effect on E-commerce adoption, followed by management support and external pressure. Moreover, external support only has minor impact on E-commerce adoption in the Covid-19. Meaningfully, this study makes contribution to both innovation literature and practical management with new insight of current Vietnamese situation for small and medium organizations.

Agricultural wastes rich in β-mannan are an important environmental problem in tropical and sub-tropical countries. This research aims at dealing with this and investigates the valorization of mannan-rich copra meal from virgin coconut oil manufacturing into mannan-oligosaccharides (β-MOS) by enzymatic hydrolysis using β-mannanase from Bacillus licheniformis ( Bl Man26B). Lab-scale process, involving pre-treatment and bioconversion steps, were conducted and evaluated. Lyophilized β-MOS was analyzed and its biological activities were assessed. The size of oligosaccharides obtained ranged from dimers to hexamers with 36.7% conversion yields. The prebiotic effects of β-MOS were demonstrated in comparison with commercial inulin and fructo-oligosaccharides (FOS). In vitro toxicity assays of β -MOS on human dermal fibroblasts and monocytes showed no cytotoxic effect. Interestingly, β-MOS at concentrations ranging from 10 to 200 µg/mL also demonstrated potent anti-inflammatory activity against LPS-induced inflammation of human macrophage THP-1 in a dose-dependent manner. However, at high dose, β-MOS could also stimulate inflammation. Therefore, further investigation must be conducted to ensure its efficacy and safe use in the future. These results indicate that β-MOS have the potential to be used as valued-added health-promoting nutraceutical or feed additive after additional in-depth studies. These finding should be applicable for other agricultural wastes rich in mannan as well.

Background The present study aimed to identify and critically appraise the quality of model-based economic evaluation studies in mental health prevention. Methods A systematic search was performed on MEDLINE, EMBASE, EconLit, PsycINFO, and Web of Science. Two reviewers independently screened for eligible records using predefined criteria and extracted data using a pre-piloted data extraction form. The 61-item Philips Checklist was used to critically appraise the studies. Systematic review registration number : CRD42020184519. Results Forty-nine studies were eligible to be included. Thirty studies (61.2%) were published in 2015–2021. Forty-seven studies were conducted for higher-income countries. There were mainly cost-utility analyses ( n  = 31) with the dominant primary outcome of quality-adjusted life year. The most common model was Markov ( n  = 26). Most of the studies were conducted from a societal or health care perspective ( n  = 37). Only ten models used a 50-year time horizon ( n  = 2) or lifetime horizon ( n  = 8). A wide range of mental health prevention strategies was evaluated with the dominance of selective/indicate strategy and focusing on common mental health problems (e.g., depression, suicide). The percentage of the Philip checkilst’s criteria fulfilled by included studies was 69.3% on average and ranged from 43.3 to 90%. Among three domains of the Philip checklist, criteria on the model structure were fulfilled the most (72.1% on average, ranging from 50.0% to 91.7%), followed by the data domain (69.5% on average, ranging from 28.9% to 94.0%) and the consistency domain (54.6% on average, ranging from 20.0% to 100%). The practice of identification of ‘relevant’ evidence to inform model structure and inputs was inadequately performed. The model validation practice was rarely reported. Conclusions There is an increasing number of model-based economic evaluations of mental health prevention available to decision-makers, but evidence has been limited to the higher-income countries and the short-term horizon. Despite a high level of heterogeneity in study scope and model structure among included studies, almost all mental health prevention interventions were either cost-saving or cost-effective. Future models should make efforts to conduct in the low-resource context setting, expand the time horizon, improve the evidence identification to inform model structure and inputs, and promote the practice of model validation.

Lactose is a major disaccharide by-product from the dairy industries, and production of whey alone amounts to about 200 million tons globally each year. Thus, it is of particular interest to identify improved enzymatic processes for lactose utilization. Microbial β-glucosidases (BGL) with significant β-galactosidase (BGAL) activity can be used to convert lactose to glucose (Glc) and galactose (Gal), and most retaining BGLs also synthesize more complex sugars from the monosaccharides by transglycosylation, such as galacto-oligosaccharides (GOS), which are prebiotic compounds that stimulate growth of beneficial gut bacteria. In this work, a BGL from the thermophilic and halophilic bacterium Halothermothrix orenii, HoBGLA, was characterized biochemically and structurally. It is an unspecific β-glucosidase with mixed activities for different substrates and prominent activity with various galactosidases such as lactose. We show that HoBGLA is an attractive candidate for industrial lactose conversion based on its high activity and stability within a broad pH range (4.5–7.5), with maximal β-galactosidase activity at pH 6.0. The temperature optimum is in the range of 65–70 °C, and HoBGLA also shows excellent thermostability at this temperature range. The main GOS products from HoBGLA transgalactosylation are β-D-Galp-(1→6)-D-Lac (6GALA) and β-D-Galp-(1→3)-D-Lac (3GALA), indicating that D-lactose is a better galactosyl acceptor than either of the monosaccharides. To evaluate ligand binding and guide GOS modeling, crystal structures of HoBGLA were determined in complex with thiocellobiose, 2-deoxy-2-fluoro-D-glucose and glucose. The two major GOS products, 3GALA and 6GALA, were modeled in the substrate-binding cleft of wild-type HoBGLA and shown to be favorably accommodated.

See the retraction notice E3S Web of Conferences 420 , 00001 (2023), https://doi.org/10.1051/e3sconf/202342000001

Autophagy is an essential quality control mechanism for maintaining organellar functions in eukaryotic cells. Defective autophagy in pancreatic beta cells has been shown to be involved in the progression of diabetes through impaired insulin secretion under glucolipotoxic stress. The underlying mechanism reveals the pathologic role of the hyperactivation of mechanistic target of rapamycin (mTOR), which inhibits lysosomal biogenesis and autophagic processes. Moreover, accumulating evidence suggests that oxidative stress induces Ca 2+ depletion in the endoplasmic reticulum (ER) and cytosolic Ca 2+ overload, which may contribute to mTOR activation in perilysosomal microdomains, leading to autophagic defects and β-cell failure due to lipotoxicity. This review delineates the antagonistic regulation of autophagic flux by mTOR and AMP-dependent protein kinase (AMPK) at the lysosomal membrane, and both of these molecules could be activated by perilysosomal calcium signaling. However, aberrant and persistent Ca 2+ elevation upon lipotoxic stress increases mTOR activity and suppresses autophagy. Therefore, normalization of autophagy is an attractive therapeutic strategy for patients with β-cell failure and diabetes. Autophagy defects: the hidden culprit in diabetes progression Excessive intake of fatty acids can result in a condition known as lipotoxicity (harmful effect of fats on cells), which can harm pancreatic beta cells (cells that produce insulin) and contribute to type 2 diabetes. Researchers have found that this harm is due to a disturbance in the cells' autophagy process (a system used by cells to eliminate unnecessary or dysfunctional parts). Specifically, the research revealed that the autophagy process is hindered by the activation of a protein complex called mTORC1 and the suppression of a protein named AMPK. These proteins control the autophagy process and their disturbance leads to the buildup of harmful substances in the cell, causing cell death. The researchers propose that future treatment strategies could focus on restoring the balance of these proteins to safeguard pancreatic beta cells from lipotoxicity. This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.

Platinum-based antitumor agents have been widely used to treat head and neck squamous cell carcinoma (HNSCC) and numerous other malignancies. Cisplatin is the most frequently used platinum-based antitumor agent, however drug resistance and numerous undesirable side effects limit its clinical efficacy for cancer patients. Cancer cells discharge cisplatin into the extracellular space via copper transporters such as ATPase copper transporting beta (ATP7B) in order to escape from cisplatin-induced cell death. In the present study, it was demonstrated for the first time that the copper chelator ammonium tetrathiomolybdate (TM) has several promising effects on cisplatin and HNSCC. First, TM suppressed the ATP7B expression in HNSCC cell lines in vitro, thereby enhancing the accumulation and apoptotic effect of cisplatin in the cancer cells. Next, it was revealed that TM enhanced the antitumor effect of cisplatin in HNSCC cell tumor progression in a mouse model of bone invasion, which is important since HNSCC cells frequently invade to facial bone. Finally, it was demonstrated that TM was able to overcome the cisplatin resistance of a human cancer cell line, A431, via ATP7B depression in vitro.

β-Galactosidase encoding genes lacLM from Lactobacillus helveticus DSM 20075 were cloned and successfully overexpressed in Escherichia coli and Lactobacillus plantarum using different expression systems. The highest recombinant β-galactosidase activity of ∼26 kU per L of medium was obtained when using an expression system based on the T7 RNA polymerase promoter in E. coli, which is more than 1000-fold or 28-fold higher than the production of native β-galactosidase from L. helveticus DSM 20075 when grown on glucose or lactose, respectively. The overexpression in L. plantarum using lactobacillal food-grade gene expression system resulted in ∼2.3 kU per L of medium, which is approximately 10-fold lower compared to the expression in E. coli. The recombinant β-galactosidase from L. helveticus overexpressed in E. coli was purified to apparent homogeneity and subsequently characterized. The Km and vmax values for lactose and o-nitrophenyl-β-d-galactopyranoside (oNPG) were 15.7 ± 1.3 mM, 11.1 ± 0.2 µmol D-glucose released per min per mg protein, and 1.4 ± 0.3 mM, 476 ± 66 µmol o-nitrophenol released per min per mg protein, respectively. The enzyme was inhibited by high concentrations of oNPG with Ki,s = 3.6 ± 0.8 mM. The optimum pH for hydrolysis of both substrates, lactose and oNPG, is pH 6.5 and optimum temperatures for these reactions are 60 and 55 °C, respectively. The formation of galacto-oligosaccharides (GOS) in discontinuous mode using both crude recombinant enzyme from L. plantarum and purified recombinant enzyme from E. coli revealed high transgalactosylation activity of β-galactosidases from L. helveticus; hence, this enzyme is an interesting candidate for applications in lactose conversion and GOS formation processes.

Vascular calcification is a serious complication of hyperphosphatemia that causes cardiovascular morbidity and mortality. Previous studies have reported that plasmalemmal phosphate (Pi) transporters, such as PiT-1/2, mediate depolarization, Ca 2+ influx, oxidative stress, and calcific changes in vascular smooth muscle cells (VSMCs). However, the pathogenic mechanism of mitochondrial Pi uptake in vascular calcification associated with hyperphosphatemia has not been elucidated. We demonstrated that the phosphate carrier (PiC) is the dominant mitochondrial Pi transporter responsible for high Pi-induced superoxide generation, osteogenic gene upregulation, and calcific changes in primary VSMCs isolated from rat aortas. Notably, acute incubation with high Pi markedly increased the protein abundance of PiC via ERK1/2- and mTOR-dependent translational upregulation. Genetic suppression of PiC prevented Pi-induced ERK1/2 activation, superoxide production, osteogenic differentiation, and vascular calcification of VSMCs in vitro and aortic rings ex vivo. Pharmacological inhibition of mitochondrial Pi transport using butyl malonate (BMA) or mersalyl abolished all pathologic changes involved in high Pi-induced vascular calcification. BMA or mersalyl also effectively prevented osteogenic gene upregulation and calcification of aortas from 5/6 subtotal nephrectomized mice fed a high-Pi diet. Our results suggest that mitochondrial Pi uptake via PiC is a critical molecular mechanism mediating mitochondrial superoxide generation and pathogenic calcific changes, which could be a novel therapeutic target for treating vascular calcification associated with hyperphosphatemia. Vascular disease: Phosphate transport protein implicated in blood vessel stiffening Drugs that block the transport of phosphate ions into mitochondria, the ‘powerhouses’ of the cell, could prevent life-threatening stiffening of blood vessel walls. Using smooth muscle cells taken from rat aortas, Kyu-Sang Park of Yonsei University Wonju College of Medicine, South Korea, and colleagues showed how mitochondrial uptake of phosphate via phosphate transport proteins triggered toxic metabolite generation, increased activity of bone formation genes and other reactions that collectively drive the deposition of minerals, leading to vascular stiffening. Suppression of the proteins’ activity, either using drug-like compounds or by genetic means, reduced these pathological changes in mice. The findings highlight the therapeutic potential of such an approach in people with elevated serum phosphate leading to calcium build-up within their vessel walls, a major risk factor for cardiovascular disease.