Enhanced methane production from waste activated sludge by microbial electrolysis cell assisted anaerobic digestion: Fate and effect of humic substances.

Humic substances as major components of waste activated sludge are refractory to degrade and have inhibition in traditional anaerobic digestion (AD). This study for the first time investigated the feasibility and mechanism of microbial electrolysis cell assisted anaerobic digestion (MEC-AD) to break the recalcitrance and inhibition of humic substances. The cumulative methane production of AD decreased from 134.7 to 117.6 mL/g-VS with the addition of humic acids and fulvic acids at 25.2-102.1 mg/g-VS. However, 0.6 V MEC-AD maintained stable methane production (155.5-158.2 mL/g-VS) under the effect of humic substances. 0.6 V MEC-AD formed electrical stimulation on microbial cells, provided anodic oxidation and cathodic reduction transformation pathways for humic substances (acting as carbon sources and electron shuttles), and aggregated functional microorganisms on electrodes, facilitating the degradation of humic substances and generation of methane. This study provides a theoretical basis for improving the energy recovery and system stability of sludge treatment.

Rhamnolipid increases H2S generation from waste activated sludge anaerobic fermentation: An overlooked concern.

Rhamnolipid (RL), one representative biosurfactant, is widely regarded as an economically feasible and environmentally beneficial additive to improve fermentation efficiency and resource recovery from waste activated sludge (WAS). However, its potentially detrimental impact on WAS fermentation such as H2S generation was overlooked previously. This study therefore aims to fill the gap through exploring whether and how the presence of RL affects H2S generation from WAS anaerobic fermentation. Experimental results showed that when RL increased from 0 to 40 mg/g total suspended solids (TSS), the cumulative H2S yield enhanced from 323.6 ×  10-4 to 620.3 ×  10-4 mg/g volatile suspended solids (VSS). Mechanism analysis showed that RL reduced WAS surface tension, which benefited transformations of organic sulfurs (e.g., aliphatic-S and sulfoxide) and inorganic sulfate from solid to liquid phase. The presence of RL not only reduced the ratio of α-helix/(ß-sheet + random coil) and damaged the hydrogen bonding networks of organic sulfurs but also promoted substrate surface charges and cell membrane permeability. These facilitated the contact between hydrolase and organic sulfurs, thereby increasing sulfide production from organic sulfurs hydrolysis. Further investigations showed that RL promoted the expression of key genes (e.g., aprA/B and dsrA/B) involved in the dissimilatory sulfate reduction, which accelerated the reaction of adenosine 5'-phosphosulfate (APS)→ sulfite→ sulfide. Meanwhile, RL inhibited the corresponding key genes such as CysH, and Sir, responsible for assimilatory sulfate reduction (APS→3'-phosphoadenosine-5'phosphosulfate→organosulfur), which reduced substrate competition in favor of H2S production from dissimilatory sulfate reduction. Besides, RL decreased the fermentation pH, which benefited the transformation of HS- to H2S.

Effect of sulfamethoxazole and oxytetracycline on enhanced biological phosphorus removal and bacterial community structure.

The individual and combined effects of sulfamethoxazole (SMX) and oxytetracycline (OTC) on an enhanced biological phosphorus removal (EBPR) system was investigated. OTC at 5 mg/L resulted in filamentous bulking with a collapse of EBPR system. P removal decreased to 44.8% and COD was mostly removed during the aerobic phase. SMX and OTC had antagonistic effects in EBPR system. The inhibitory effect of SMX and SMX + OTC on P removal, COD removal, glycogen transformation and extracellular polymeric substances content was reversible with prolonged operation, accompanied with increase of polyphosphate accumulating organisms. The presence of nitrification inhibitor allylthiourea, high pH and low tetX abundance limited the removal of SMX and OTC. The bacterial community structure, antibiotic resistance genes abundances and genes functions were also investigated by metagenomic analysis. The results of this study offer insights into the individual and combined environmental risks of SMX and OTC, and their impact on EBPR.

Identification of a Novel NF1 Frameshift Variant in a Chinese Family with Neurofibromatosis Type 1.

Neurofibromatosis type 1 (NF1) is a progressive neurocutaneous disorder in humans, mainly characterized by café-au-lait macules (CALMs) and neurofibromas. NF1 is caused by variants of the neurofibromin 1 gene (NF1), which encodes a Ras-GTPase-activating protein called neurofibromin. NF1 variants may result in loss of neurofibromin function and elevation of cell proliferation and tumor formation. In this study, a Chinese NF1 family with an autosomal dominant inheritance pattern was recruited. Exome sequencing and Sanger sequencing were performed to discover the causative variant responsible for the family, followed by molecular analysis of effect of the mutated NF1 protein on Ras activity. A novel frameshift variant c.541dupC (p.(Gln181Profs∗20)) in the NF1 gene was identified in all three affected family members. The variant cosegregated with the disease phenotypes in the pedigree and was absent in 100 healthy controls. Bioinformatic analysis showed that the variant c.541dupC (p.(Gln181Profs∗20)) was pathogenic. The further molecular analysis verified the cells expressing NF1 variant p.(Gln181Profs∗20) partially enhanced Ras activity and elevated cell proliferation and tumor formation due to loss of neurofibromin function caused by the variant. Taken together, the data strongly advocate the c.541dupC (p.(Gln181Profs∗20)) variant as the underlying genetic cause of the Chinese family with NF1. Moreover, our findings broaden the spectrum of NF1 variants and provide molecular insights into the pathogenesis of NF1.

Injury in Minipig Parotid Glands following Fractionated Exposure to 30 Gy of Ionizing Radiation.

OBJECTIVE: To explore the effects of 30 Gy of (60)Co γ-rays on apoptosis and reactive oxygen species (ROS) levels in minipig parotid cells as a possible mechanism for radiation-induced parotid injury. STUDY DESIGN: Experimental study. SETTING: Department of Radiotherapy, First Affiliated Hospital, Guangxi Medical University, Nanning, China. SUBJECTS AND METHODS: Forty male minipigs were divided into control and irradiated groups. Terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick-end labeling was used for detecting apoptosis in the parotid cells, immunohistochemistry, and western blots were used to test expression of the B-cell lymphoma 2 (Bcl-2) and BCL2-associated X (Bax) proteins, and reverse transcription polymerase chain reaction was used to analyze the expression of Bcl-2, Bax, p53, and caspase-3 messenger ribonucleic acid. An enzyme-linked immunosorbent assay was used to detect ROS levels in the parotid tissue. RESULTS: At each time point, the apoptotic rates in the irradiated group were higher than those in the control group. Furthermore, the ROS and expression levels of Bax, p53, and caspase-3 messenger ribonucleic acid and proteins gradually increased and were higher than those in the control group. Conversely, the expression of Bcl-2 was decreased in the irradiated group (P < .05). CONCLUSIONS: Ionizing radiation induces the production of ROS and promotes changes in the expression of several apoptotic proteins, which increases apoptosis and likely contributes to the mechanism of radiation-induced parotid injury.

N-Heteroarylmethyl-5-hydroxy-1,2,5,6-tetrahydropyridine-3-carboxylic acid a novel scaffold for the design of uncompetitive α-glucosidase inhibitors.

The enzyme α-glucosidase has attracted interest owing to its involvement in the digestive process of carbohydrate, its role in intracellular glycoprotein trafficking, tumorigenesis and viral infection. In this study, several members of a new family of N-heteroarylmethyl substituted azasugars were synthesized and evaluated as α-glucosidase inhibitors. We systematically investigated the effect of different N-substituents as well as the role of hydroxyl and carboxylate moieties on the piperidine ring. The compounds N-heteroarylmethyl-5-hydroxy-1,2,5,6-tetrahydropyridine-3-carboxylic acid emerged as potent α-glucosidase inhibitors. Unlike Acarbose and other clinically relevant α-glucosidase inhibitors, these compounds act through a reversible uncompetitive mechanism of inhibition which make them attractive candidates for drug development.