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This article summarizes the nursing measures for a patient with dry eyes caused by mites treated by eye thunder fire moxibustion combined with Traditional Chinese Medicine(TCM) atomization fumigation. Key issues of nursing included eye moxibustion, TCM atomization fumigation, meibomian gland massage, TCM scrubbing and routine life, medication, diet and emotional care. Eye thunder fire moxibustion combined with TCM atomization fumigation can achieve the effect of removing insects and soft fat, generating fluid and moistening dryness. Through dialectical nursing and targeted nursing intervention, It plays an active role in relieving clinical symptoms and promoting disease recovery. (本文总结了1例眼部雷火灸联合中医雾化熏蒸治疗螨虫性干眼患者的护理经验, 通过开展眼部雷火灸疗法、中药雾化熏蒸、睑板腺按摩、中药擦洗及常规的生活、用药、饮食和情志护理干预, 达到驱虫软脂, 生津润燥的作用, 有效地改善了患者的干眼症状。)

This paper summarized the auricular acupoint pressing therapy an nursing measures for insomnia in a patient with central retinal artery occlusion. On the basis of nursing risk assessment, Traditional Chinese Medicine auricular acupoint pressing therapy was adopted. Comprehensive nursing interventions such as strengthening cooperation between medical and nursing care, providing oxygen therapy according to the doctor's advice, enhancing the psychological care and diet care of patients were carried out during the treatment. Traditional Chinese Medicine auricular acupoint pressing therapy can effectively relieve the psychological stress and improve the sleep quality of the patient. (本文总结1例采用耳穴压丸治疗视网膜中央动脉阻塞(CRAO)后失眠的护理经验。在完善护理评估的基础上, 采用中医耳穴压丸治疗, 同时积极配合医生进行救治, 遵医嘱及时给予安全的氧疗护理, 加强患者的心理护理和饮食护理, 有助于缓解患者心理压力, 改善睡眠质量。)

Diabetic nephropathy is one of the common microvascular complications in patients with diabetes, which is difficult to treat clinically, and is also a common cause of end-stage renal failure. This article discussed the long-term care of patients with diabetic nephropathy and its research progress, including the risk factors of diabetic nephropathy and nursing measures, in order to provide a reference for the nursing of diabetic nephropathy, so as to improve the quality of life of diabetic nephropathy population. (糖尿病肾病是糖尿病患者常见的微血管并发症之一, 临床治疗相对困难, 也是导致患者发生终末期肾功能衰竭的常见病因。本文探讨了糖尿病肾病患者长期护理及其研究进展, 包括糖尿病肾病的危险因素和对应护理措施等, 旨在为糖尿病肾病的护理提供参考, 以改善糖尿病肾病人群的生命质量。)

This paper reviewed the ear-apex bloodletting therapy and nursing management for a patient with hordeolum. According to the patient’s evaluation results, the treatment problems were pointed out, and individualized Traditional Chinese Medicine treatment methods were formulated, including emotional management, dietary care, daily life management, drug care, etc. , Traditional Chinese Medicine by syndrome differentiation is aimed to to change the patient’s condition, promote the recovery and improve the quality of life of the patient. (回顾性分析1例麦粒肿患者的临床资料, 总结耳尖放血的效果和相关护理措施。根据评估结果明确治疗和护理问题, 制定个体化中医治疗和护理方案, 在耳尖放血治疗的基础上, 实施情志护理、膳食护理、日常生活管理、药物护理等。通过中医辨证施护改善临床症状, 促进病情痊愈, 改善患者生活质量。)

β‐Nicotinamide mononucleotide (NMN) is a biologically active nucleotide that regulates the physiological metabolism of the body by rapidly increasing nicotinamide adenine dinucleotide (NAD+). To determine the safety and biological activity of NMN resources, we constructed a recombinant strain of P. pastoris that heterologously expresses nicotinamide‐phosphate ribosyltransferase (NAMPT), and subsequently catalyzed and purified the expressed product to obtain NMN. Consequently, this study established a high‐fat diet (HFD) obese model to investigate the lipid‐lowering activity of NMN. The findings showed that NMN supplementation directly increased the NAD+ levels, and reduced HFD‐induced liver injury and lipid deposition. NMN treatment significantly decreased total cholesterol (TC) and triglyceride (TG) in serum and liver, as well as alanine aminotransferase (ALT) and insulin levels in serum (p <.05 or p <.01). In conclusion, this study combined synthetic biology with nutritional evaluation to confirm that P. pastoris‐generated NMN modulated lipid metabolism in HFD mice, offering a theoretical framework and evidence for the application of microbially created NMN. Significance statement: The application of β‐Nicotinamide mononucleotide (NMN) faces challenges in the food and pharmaceutical industries due to safety concerns in its production, and the role of NMN in the regulation of lipid metabolism in a high‐fat diet (HFD) model is unclear. In this article, a recombinant strain of P. pastoris that heterologously expresses nicotinamide‐phosphate ribosyltransferase (NAMPT) was constructed, and NMN yield of 1.46 mg/g DCW was obtained by methanol induction of P. pastoris. Furthermore, this study found that supplementation with microbial‐derived NMN reduced liver injury and lipid deposition in HFD mice. [ABSTRACT FROM AUTHOR]

Objective To determine whether metformin(Met) inhibits the proliferation of colorectal cancer cells by inducing cell senescence, and to preliminarily explore the underlying mechanism. Methods LOVO and SW480 colorectal cancer cells were treated with different concentrations of Met(0, 2.5, 5.0, 10.0, 20.0 and 40.0 mmol/L). The cell viability was detected by CCK-8 assay, and apoptosis and cell cycle were detected by flow cytometry. According to the results of apoptosis, differences between control group (0 mmol/L) and 5.0 mmol/L Met group(n=3) were compared in following experiments. Cell proliferation was detected by CCK-8 assay, EdU assay, and clone formation assay, senescence metabolism was detected by senescence-associated β-galactosidase(SA-β-gal)staining, protein phosphatase 2A(PP2A) enzyme activity was measured with ELASA, and protein expression was detected with Western blotting. PP2A inhibitor LB-100 was used to treat the cells alone or combined with Met, and then the cells were divided into control group, Met group, Met+LB-100 group, and LB-100 group(n=3). Above experiments were performed again. Results Met treatment significantly inhibited LOVO and SW480 cells proliferation in a concentration- and time-dependent manner(P < 0.05). Under the treatment of low concentration(≤5.0 mmol/L) of Met, the cells presented no obvious apoptosis, but were obviously inhibited for proliferation and arrested at G0/G1 phase. The cells displayed a typical senescence-like morphology of large, flat and vacuolated, and the number of SA-β-gal positive cells was increased significantly. For PP2A, total protein expression showed no change, but phosphorylation level decreased obviously and PP2A activity increased statistically(P < 0.05), in the meantime, the phosphorylation level of downstream AKT protein decreased and senescence-related proteins p53 and P21 increased significantly. Treatment by PP2A inhibitor LB-100 combined with Met significantly reversed the inhibition of Met on cell proliferation and delayed Met-induced cell senescence. Conclusion Low concentration of Met can induce cell senescence through PP2A/AKT pathway and then inhibit the proliferation of colorectal cancer cells.

Luminescent materials with emissions at specific wavelengths, which have a relatively lower proportion of emissions in the solar spectrum, have great prospects for use in production and daily life. In this study, SrGaB2O7 deep‐blue phosphors doped with Bi3+ are synthesized, it has 430 nm deep‐blue emissions and a low proportion of emissions relative to 470–660 nm visible light in the solar spectrum. By co‐doping with alkali metal ions to compensate for the charge, the emission intensities and absolute quantum yields of the phosphors can be effectively improved. The SrGaB2O7:0.01Bi3+, 0.01K+ deep‐blue phosphor has a high quantum yield of 85% and negative thermal quenching properties. Moreover, the SrGaB2O7:0.01Bi3+, 0.01K+ deep‐blue phosphor can be packaged with different potting adhesives to form light‐emitting diodes (LEDs), exhibiting excellent luminescent performances and promising application prospects. [ABSTRACT FROM AUTHOR]

Under normal physiological conditions, reactive oxygen species (ROS) are produced through redox reactions as byproducts of respiratory and metabolic activities. However, due to various endogenous and exogenous factors, the body may produce excessive ROS, which leads to oxidative stress (OS). Numerous studies have shown that OS causes a variety of pathological changes in cells, including mitochondrial dysfunction, DNA damage, telomere shortening, lipid peroxidation, and protein oxidative modification, all of which can trigger apoptosis and senescence. OS also induces a variety of aging-related diseases, such as retinal disease, neurodegenerative disease, osteoarthritis, cardiovascular diseases, cancer, ovarian disease, and prostate disease. In this review, we aim to introduce the multiple internal and external triggers that mediate ROS levels in rodents and humans as well as the relationship between OS, aging, and aging-related diseases. Finally, we present a statistical analysis of effective antioxidant measures currently being developed and applied in the field of aging research. [ABSTRACT FROM AUTHOR]