Study on the fermentation effect of Rhodotorula glutinis utilizing tofu whey wastewater and the influence of Rhodotorula glutinis on laying hens

BackgroundTofu whey wastewater (TWW) is the wastewater of tofu processing, which is rich in a variety of nutrients. Rhodotorula glutinis can make full use of TWW to ferment and reproduce yeast cells, produce carotenoids and other nutrients, improve the utilization value of TWW, and reduce environmental pollution and resource waste.MethodsIn this study, the nutrient composition changes of TWW treated by Rhodotorula glutinis were analyzed to reformulate TWW medium, and the optimal composition and proportion of TWW medium that can improve the biomass and carotenoids production of Rhodotorula glutinis were explored. Meanwhile, the Rhodotorula glutinis liquid obtained under these conditions was used to prepare biological feed for laying hens, and the effect of Rhodotorula glutinis growing on TWW as substrate on laying performance and egg quality of laying hens were verified.ResultsThe results showed that the zinc content of TWW after Rhodotorula glutinis fermentation increased by 62.30%, the phosphorus content decreased by 42.31%, and the contents of vitamin B1, B2 and B6 increased to varying degrees. The optimal fermentation conditions of Rhodotorula glutinis in the TWW medium were as follow: the initial pH was 6.40, the amount of soybean oil, glucose and zinc ions was 0.80 ml/L, 16.32 g/L, and 20.52 mg/L, respectively. Under this condition, the biomass of Rhodotorula glutinis reached 2.23 g/L, the carotenoids production was 832.86 μg/g, and the number of effective viable yeast count was 7.08 × 107 cfu/ml. In addition, the laying performance and egg quality of laying hens fed Rhodotorula glutinis biological feed were improved.DiscussionIn this study, we analyzed the composition changes of TWW, optimized the fermentation conditions of Rhodotorula glutinis in TWW medium, explored the influence of Rhodotorula glutinis utilizing TWW on laying layers, and provided a new idea for the efficient utilization of TWW

Association of tea and its extracts with colorectal adenomas: meta-analysis and systematic review

BackgroundThere are many studies on the association of tea and its extracts with colorectal adenomas, but the results have varied. The study aims to investigate the effect of tea and its extracts on colorectal adenomas using meta analysis and systematic review.MethodsLiterature was obtained through PubMed, Cochrane Library, Embase and Chinese BioMedical Literature Service System since the establishment of the database until April 31, 2023. Search terms include adenomas, polyps, colorectal, rectal, rectum, tea, epigallocatechin, drinking and beverages. Meta-regression analysis was used to infer the source of heterogeneity. Heterogeneity was assessed using I2 statistics and Q test. The effect measures were odds ratio (OR) and 95% confidence interval (95% CI). Stata17.0 software was used for data processing.ResultsThe findings indicated that study design (t = 0.78, P = 0.454), types of tea intake (t = 1.35, P = 0.205), occurrences (t = -0.19, P = 0.852), regions (t = 1.13, P = 0.281) and grades of adenomas (t = 0.06, P = 0.952) were statistical homogeneity. Tea and its extracts were negatively correlated with the risk of colorectal adenomas (OR = 0.81, 95% CI: 0.66–0.98). No publication bias was found in this study (t = -0.22, P = 0.828) and the results are robust.ConclusionThis study suggests that tea and its extracts have a certain protective effect on colorectal adenomas, which provides scientific evidence for preventive strategies for colorectal adenomas. As for the causal relationship between tea and its extracts on colorectal adenomas, further prospective studies are needed

Nitrogen/sulfur dual-doping of reduced graphene oxide harvesting hollow ZnSnS3 nano-microcubes with superior sodium storage

Bimetallic sulfides have exhibited promising applications in advanced sodium-ion batteries (SIBs) due to their relatively high electronic conductivity and electrochemical activity. In this study, for the first time, the N/S dual-doped reduced graphene oxide (rGO) encapsulating hollow ZnSnS3 nano-microcubes (N/S-rGO@ZnSnS3) is designed to improve the sluggish reaction kinetics, poor cycling stability and unsatisfactory rate capability of metal sulfides. To examine this design, the cycling stability and rate capability of the desired anode material is studied in detail. It is found that N/S-rGO@ZnSnS3 hybrid delivers a high discharge capacity of 501.7 mAh g−1 after 100 cycles at 0.1 A g−1, and a reversible capacity of 290.7 mAh g−1 after 500 cycles at 1.0 A g−1 with a capacity fading of 0.06% per cycle. The cycling stability as well as rate capability of N/S-rGO@ZnSnS3 are superior to those of the pristine hollow ZnSnS3 cubes/un-doped rGO composite. It is convinced that the electrode performance is strongly rooted in its structural conformation. Furthermore, the structural evolutions of ZnSnS3 reactions with sodium are revealed by in situ X-ray diffraction combined with ex situ X-ray photoelectron spectroscopy, which provides a valuable revelation for the understanding of reaction mechanism toward bimetallic sulfides and beyond

SiO2 nanoparticles induce cytotoxicity and protein expression alteration in HaCaT cells

<p>Abstract</p> <p>Background</p> <p>Nanometer silicon dioxide (nano-SiO₂) has a wide variety of applications in material sciences, engineering and medicine; however, the potential cell biological and proteomic effects of nano-SiO₂exposure and the toxic mechanisms remain far from clear.</p> <p>Results</p> <p>Here, we evaluated the effects of amorphous nano-SiO₂(15-nm, 30-nm SiO₂). on cellular viability, cell cycle, apoptosis and protein expression in HaCaT cells by using biochemical and morphological analysis, two-dimensional differential gel electrophoresis (2D-DIGE) as well as mass spectrometry (MS). We found that the cellular viability of HaCaT cells was significantly decreased in a dose-dependent manner after the treatment of nano-SiO₂and micro-sized SiO₂particles. The IC₅₀value (50% concentration of inhibition) was associated with the size of SiO₂particles. Exposure to nano-SiO₂and micro-sized SiO₂particles also induced apoptosis in HaCaT cells in a dose-dependent manner. Furthermore, the smaller SiO₂particle size was, the higher apoptotic rate the cells underwent. The proteomic analysis revealed that 16 differentially expressed proteins were induced by SiO₂exposure, and that the expression levels of the differentially expressed proteins were associated with the particle size. The 16 proteins were identified by MALDI-TOF-TOF-MS analysis and could be classified into 5 categories according to their functions. They include oxidative stress-associated proteins; cytoskeleton-associated proteins; molecular chaperones; energy metabolism-associated proteins; apoptosis and tumor-associated proteins.</p> <p>Conclusions</p> <p>These results showed that nano-SiO₂exposure exerted toxic effects and altered protein expression in HaCaT cells. The data indicated the alterations of the proteins, such as the proteins associated with oxidative stress and apoptosis, could be involved in the toxic mechanisms of nano-SiO₂exposure.</p

Pathological Comparisons of the Hippocampal Changes in the Transient and Permanent Middle Cerebral Artery Occlusion Rat Models

© Copyright © 2019 Shah, Li, Kury, Zeb, Khatoon, Liu, Yang, Liu, Yao, Khan, Koh, Jiang and Li. Ischemic strokes are categorized by permanent or transient obstruction of blood flow, which impedes delivery of oxygen and essential nutrients to brain. In the last decade, the therapeutic window for tPA has increased from 3 to 5–6 h, and a new technique, involving the mechanical removal of the clot (endovascular thrombectomy) to allow reperfusion of the injured area, is being used more often. This last therapeutic approach can be done until 24 h after stroke onset. Due to this fact, more acute ischemic stroke patients are now being recanalized, and so tMCAO is probably the “best” model to address these patients that have a potential good outcome in terms of survival and functional recovery. However, permanent occlusion patients are also important, not only to increase survival rate but also to improve functional outcomes, although these are more difficult to achieve. So, both models are important, and which target different stroke patients in the clinical scenario. Hippocampus has a vital role in memory and cognition, is prone to ischemic induced neurodegeneration. This study was designed to delineate the molecular, pathological, and neurological changes in rat models of t-MCAO, permanent MCAO (pMCAO), and pMCAO with diabetic conditions in hippocampal tissue. Our results showed that these three models showed distinct discrepancies at numerous pathological process, including key signaling molecules involved in neuronal apoptosis, glutamate induced excitotoxicity, neuroinflammation, oxidative stress, and neurotrophic changes. Our result suggests that the two commonly used MCAO models exhibited tremendous differences in terms of neuronal cell loss, glutamate excitotoxic related signaling, synaptic transmission markers, neuron inflammatory and oxidative stress molecules. These differences may reflect the variations in different models, which may provide valuable information for mechanistic and therapeutic inconsistences as experienced in both preclinical models and clinical trials

Ginsenoside Rg1 Ameliorates Behavioral Abnormalities and Modulates the Hippocampal Proteomic Change in Triple Transgenic Mice of Alzheimer’s Disease

Alzheimer’s disease (AD) is one of the most common neurodegenerative diseases, so far, there are no effective measures to prevent and cure this deadly condition. Ginsenoside Rg1 (Rg1) was shown to improve behavioral abnormalities in AD; however, the potential mechanisms remain unclear. In this study, we pretreated 7-month-old 3xTg-AD mice for 6 weeks with Rg1 and evaluated the effects of Rg1 on the behaviors and the protein expression of hippocampal tissues. The behavioral tests showed that Rg1 could improve the memory impairment and ameliorate the depression-like behaviors of 3xTg-AD mice. Proteomic results revealed a total of 28 differentially expressed hippocampal proteins between Rg1-treated and nontreated 3xTg-AD mice. Among these proteins, complexin-2 (CPLX2), synapsin-2 (SYN2), and synaptosomal-associated protein 25 (SNP25) were significantly downregulated in the hippocampus of 3xTg-AD mice compared with the WT mice, and the treatment of Rg1 modulated the expression of CPLX2 and SNP25 in the hippocampus of 3xTg-AD mice. The expression of CPLX2, SYN2, and SNP25 was further validated by Western blot analysis. Taken together, we concluded that Rg1 could be a potential candidate drug to improve the behavioral deficits in AD via modulating the expression of the proteins (i.e., CPLX2, SYN2, and SNP25)

Melatonin Protects MCAO-Induced Neuronal Loss via NR2A Mediated Prosurvival Pathways

Stroke is the significant cause of human mortality and sufferings depending upon race and demographic location. Melatonin is a potent antioxidant that exerts protective effects in differential experimental stroke models. Several mechanisms have been previously suggested for the neuroprotective effects of melatonin in ischemic brain injury. The aim of this study is to investigate whether melatonin treatment affects the glutamate N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor signaling in cerebral cortex and striatum 24 h after permanent middle cerebral artery occlusion (MCAO). Melatonin (5 mg/kg) attenuated ischemia-induced down regulation of NMDA receptor 2 (NR2a), postsynaptic density-95 (PSD95) and increases NR2a/PSD95 complex association, which further activates the pro-survival PI3K/Akt/GSK3β pathway with mitigated collapsin response mediator protein 2 (CRMP2) phosphorylation. Furthermore, melatonin increases the expression of γ-enolase, a neurotrophic factor in ischemic cortex and striatum, and preserve the expression of presynaptic (synaptophysin and SNAP25) and postsynaptic (p-GluR1845) protein. Our study demonstrated a novel neuroprotective mechanism for melatonin in ischemic brain injury which could be a promising neuroprotective agent for the treatment of ischemic stroke

The effect of socioeconomic status on three-year mortality after first-ever ischemic stroke in Nanjing, China

BACKGROUND: Low socioeconomic status (SES) is associated with increased mortality after stroke in developed countries. This study was performed to determine whether a similar association also exists in China. METHODS: A total of 806 patients with first-ever ischemic stroke were enrolled in our study. From August 1999 to August 2005, the three-year all-cause mortality following the stroke was determined. Level of education, occupation, taxable income and housing space were used as indicators for SES. Stepwise univariate and multivariate COX proportional hazards models were used to study the association between the SES measures and the three-year mortality. RESULTS: Our analyses confirmed that occupation, taxable income and housing space were significantly associated with three-year mortality after first-ever stroke. Manual workers had a significant hazard ratio of 5.44 (95% CI 2.75 to 10.77) for death within three years when compared with non-manual workers. Those in the zero income group had a significant hazard ratio of 5.35 (95% CI 2.95 to 9.70) and those in the intermediate income group 2.10 (95% CI 1.24 to 3.58) when compared with those in the highest income group. Those in two of the three groups with the smallest housing space also had significant hazard ratios of 2.06 (95% CI 1.16 to 3.65) and 1.68 (95% CI 1.12 to 2.52) when compared with those in group with the largest housing space. These hazard ratios remained largely unchanged after multivariate adjustment for age, gender, baseline cardiovascular disease risk factors, and stroke severity. The analyses did not confirm an association with educational level. CONCLUSION: Lower SES has a negative impact on the outcome of first-ever stroke in Nanjing, China. This confirms the need to improve preventive and secondary care for stroke among low SES groups

Effects of electrolytes on the electrochemical reduction of CO2 to C2H4: a mechanistic point of view

The most attractive strategy to mitigate energy shortages and environmental pollution caused by fossil fuel consumption and CO2 emissions is to utilize renewable clean energy and convert CO2 into high value-added chemical products. However, it has been proven that activation and reduction of CO2 is a great challenge because of their thermodynamic stability and kinetic inertness. Recently, electrochemical conversion has emerged as one of the most flourishing means of converting CO2 into chemicals, ranging from common C-1 products (i.e. CO and formate) to C2+ products (i.e. ethylene, ethanol, and oxalic acid). The product distribution, i.e. the ratio of C-1 to C2+, is primarily determined by the electrode potential, cathode catalyst and electrolyte. Among them, the electrolyte plays a significant role in the total reaction efficiency and product selectivity. Here, we give a mini-review of the recently reported effects of various electrolytes on the selectivity to C2+ products (especially ethylene) in the electroreduction of CO2 and propose the mechanism of C-C coupling and possible reaction pathways, aiming to better understand the role of electrolytes in the electroreduction of CO2 to C2+ products and to provide insights into the field of process optimization for the electrochemical conversion of CO2 to high value-added chemicals and fuels. In recent years, ionic liquids have received widespread attention due to their high solubility for CO2 and the designability of their structures. They are generally considered as a green and efficient medium for homogeneous and heterogeneous catalytic reactions under ambient conditions. Here, we also briefly introduce some studies on ionic liquids used in the electrochemical reduction of CO2