Elimination of Chlorella using peracetic acid activated by dielectric barrier discharge plasma: Mechanism and cell deactivation process.

Excessive proliferation of algae in water depletes dissolved oxygen, resulting in the demise of aquatic life and environmental damage. This study delves into the effectiveness of the dielectric barrier discharge (DBD) plasma activated peracetic acid (PAA) system in deactivating Chlorella. Within 15 min, the algae removal effectiveness reached 89 % under ideal trial conditions. DBD plasma activation of PAA augmented the concentration of reactive species such as ·OH, 1O2, and organic radicals (RO·) in the solution, which are involved in the process of cell inactivation. Reactive oxygen species (ROS) within Chlorella cells continued to rise as a result of treatment-induced damage to the morphological structure and cell membrane of the organism. DNA and chlorophyll-a (Chl-a), were oxidized and destroyed by these invasive active compounds. This study presents an efficient advanced oxidation method to destroy algal cells and adds an alternative strategy for algal control in areas where eutrophication occurs.

Effect of high-quality care on limb function recovery and quality of life after osteoporotic hip fracture surgery in the elderly.

OBJECTIVES: To evaluate the effect of high-quality care on limb function recovery and quality of life (QOL) after osteoporotic hip fracture (OHF) surgery in the elderly. METHODS: 116 elderly patients with OHF enrolled in our hospital from January 2017 to December 2019 were assigned into observation group (high-quality care, n=58) and control group (routine care, n=58). After one month of intervention, Harris Hip Score (HHS) and Barthel Index (BI) were used to evaluating limb function and self-care ability, pain intensity numerical rating scale (PINRS) for pain assessment, self-rating anxiety scale (SAS), and self-rating depression scale (SDS) for emotion assessment. Besides, postsurgical complications, QOL and patient satisfaction were examined. RESULTS: HHS and BI were higher in observation group (P<0.05); PINRS, SAS and SDS were lower in observation group (P<0.05); incidence of postsurgical complications in the observation group was significantly lower than that in the control group (P<0.05); QOL and patient satisfaction in the observation group were higher than those in the control group (P<0.05). CONCLUSION: High-quality care promotes the recovery of limb function, the QOL and the satisfaction of elderly patients.

MicroRNA-497-5p stimulates osteoblast differentiation through HMGA2-mediated JNK signaling pathway.

BACKGROUND: Osteoporosis (OP) has the characteristics of the decline in bone mineral density and worsening of bone quality, contributing to a higher risk of fractures. Some microRNAs (miRNAs) have been validated as possible mediators of osteoblast differentiation. We herein aimed to clarify whether miR-497-5p regulates the differentiation of osteoblasts in MC3T3-E1 cells. METHODS: The expression of miR-497-5p in OP patients and controls was measured by RT-qPCR, and its expression changes during osteoblast differentiation were determined as well. The effects of miR-497-5p on the differentiation of MC3T3-E1 cells were studied using MTT, ALR staining, and ARS staining. The target gene of miR-497-5p was predicted by TargetScan, and the effects of its target gene on differentiation and the pathway involved were investigated. RESULTS: miR-497-5p expressed poorly in OP patients, and its expression was upregulated during MC3T3-E1 cell differentiation. Overexpression of miR-497-5p promoted mineralized nodule formation and the expression of RUNX2 and OCN. miR-497-5p targeted high mobility group AT-Hook 2 (HMGA2), while the upregulation of HMGA2 inhibited osteogenesis induced by miR-497-5p mimic. miR-497-5p significantly impaired the c-Jun NH2-terminal kinase (JNK) pathway, whereas HMGA2 activated this pathway. Activation of the JNK pathway inhibited the stimulative role of miR-497-5p mimic in osteogenesis. CONCLUSIONS: miR-497-5p inhibits the development of OP by promoting osteogenesis via targeting HMGA2.