Objective:To design and evaluate a cell membrane vaccine strategy based on dendritic cell membrane microbubbles(DCM@MBs),and to explore its potential application in tumor immunotherapy,especially the immune-specific killing of tumor cells through the activation of T cells.Methods:At first,tumor cell membrane proteins were extracted and dendritic cells(DCs)were acti-vated to confirm that tumor antigens could effectively stimulate the maturation of immature DCs.Mature DC membranes were then mixed with lipids to prepare DCM@MBs,which were characterized for morphology,size,and protein composition by confocal laser scanning microscopy and sodium dodecyl sulfate-polyacrylamide gel electrophoresis.Finally,in vitro co-culture experiments were con-ducted to assess the effect of DCM@MBs on the activation of T cells and their ability for specific killing of tumor cells.Results:In the in vitro DC activation experiment,after stimulation with tumor cell membrane proteins,the 25 μg/mL group had a significant increase in the expression level of MHC class Ⅱ molecule(25.167%±1.203%)on the surface of immature DCs compared with the control group(P<0.001),and DCM@MBs presented with microbubbles encapsulated by red cell membranes,with uniform dispersion and a size of 1-5 μm.In the in vitro co-culture experiment,the amount of breast cancer cells(9.893±0.341)%.Conclusion:The DCM@MBs strategy proposed in this study shows significant potential in tu-mor immunotherapy and can effectively activate T cells and specifically kill and eliminate tumor cells,which provides new ideas for tu-mor immunotherapy.

Since the 19th century, the emergence of model systems has helped researchers further understand cellular signaling pathways, identify potential drug targets, and conduct environmental toxicological studies. Exogenous chemicals, such as pollutants, drugs, and industrial chemicals, may affect brain biological processes and functions and eventually lead to neurological diseases. However, the brain is a complex and well-organized human organ, which is fundamentally different from any existing model system. Animal models may not be able to completely simulate the human brain in testing the neurotoxicity of environmental pollutants due to species differences. Human brain organoids, generated from human pluripotent stem cells, are emerging model systems for neurotoxicological research in line with the real situation of human body at the level of genome, transcriptome, and metabolome, and provide an effective platform for testing neurotoxicity of environmental toxins. We reviewed the latest development of brain organoids technology and its application in the evaluation of environmental neurotoxins, and provided new insights into the application of brain organoids in environmental neurotoxicology.

Objective To explore the effect of a mobile health intervention model based on self-determination theory on subthreshold depression in breast cancer patients.Methods By convenience sampling method,74 patients with breast cancer subthreshold depression who received chemotherapy in the breast department of a tertiary hospital in Guangxi from July 2021 to August 2022 were selected as the research subjects.According to the order of admission time,the patients admitted from February 2022 to August 2022 were taken as an experimental group,and the patients admitted from July 2021 to January 2022 were taken as a control group,with 37 cases in each group.On the basis of routine nursing,the experimental group implemented a mobile health intervention model based on self-determination theory.The control group received routine nursing,with every 21 days for 1 cycle and a total of 4 cycles of intervention.Before and after the intervention,the Centre for Epidemiological Studies Depression Scale(CES-D),Hamilton Rating Scale for Depression(HAMD-17),Basic Psychological Needs Satisfaction Scale(BPNS)and Functional Assessment of Cancer Therapy-Breast(FACT-B)were used to evaluate the intervention effect.Results 34 patients in the experimental group and 36 patients in the control group completed the study.After intervention,the CES-D score and HAMD-17 score of the 2 groups were lower than those before intervention(P＜0.05);the CES-D score and HAMD-17 score of the experimental group were lower than those of the control group,and the difference was statistically significant(t=7.748,P＜0.001;t=8.150,P＜0.001).The BPNS scores of the 2 groups were higher than those before the intervention,and the BPNS score of the experimental group was significantly higher than that of the control group(t=-6.534,P＜0.001).The scores of FACT-B in the 2 groups were higher than those before the intervention,and the scores of FACT-B in the experimental group were significantly higher than those in the control group(t=-4.579,P＜0.001).Conclusion The mobile health intervention model based on self-determination theory can improve the subthreshold depression,self-determination and quality of life of breast cancer patients.

Osteoarthritis （OA） is characterized by articular cartilage degeneration， synovial hyperplasia， hyperosteogeny， and narrowing of joint space， which can be caused by trauma， inflammation， and other factors. With the increasing global population aging， the incidence of OA is rising year by year， making it a major public health problem that urgently needs to be addressed. Exploring effective treatment schemes is particularly important. The pathogenesis of OA is complex， including oxidative stress， autophagy， and apoptosis. Recent studies have found that ferroptosis， a new type of cell death， is also an important pathogenic factor in OA， characterized by a series of complex changes such as iron ion accumulation， glutathione （GSH） depletion， and mitochondrial dysfunction. Research shows that inhibiting ferroptosis in chondrocytes can promote chondrocyte proliferation， delay extracellular matrix （ECM） degradation， and reduce synovial hyperplasia and inflammation. Targeting ferroptosis is a new direction in the treatment of OA. OA treatment includes intra-articular injections of steroids or hyaluronic acid and artificial joint replacement， but there are limitations. Traditional Chinese medicine （TCM） has been widely used in the treatment of various diseases because of its low cost， low drug resistance， and few side effects. Cell and animal experiments have further confirmed that TCM can intervene in the treatment of OA with ferroptosis from multiple targets， multiple levels， and aspects， but the mechanism of its treatment of OA based on ferroptosis has not been clarified. This paper discussed iron metabolism， lipid peroxidation， cysteine/glutamate transporter system Xc^- （system Xc^-）/GSH/glutathione peroxidase 4 （GPX4） pathway， nicotinamide adenine dinucleotide phosphate（NADPH）/ferroptosis suppressor protein 1 （FSP1）/coenzyme Q₁₀ （CoQ₁₀） pathway， tumor protein p53 in OA， and related molecular targets of Chinese medicine monomers and compounds on ferroptosis inhibition. Their potential therapeutic mechanisms were further analyzed to provide theoretical guidance for the treatment of OA by TCM and useful reference for the research and development of related drugs.

Skeletal muscle wasting refers to a loss of skeletal muscle mass and function.Mitochondrial quality control(MQC)is the basis by which normal physiological mitochondrial function is maintained and mainly involves the regulation of mitochondrial biogenesis,mitochondrial dynamics(fission/fusion),and mitophagy.MQC maintains muscle homeostasis by regulating the relative stability of mitochondrial shape,quantity,and quality.As an economical and effective treatment for muscular atrophy,exercise interventions are widely used,but the relationship between exercise intervention and MQC is not clear.This paper discusses the role of mitochondrial biogenesis,mitochondrial dynamics,and mitophagy in skeletal muscle atrophy and related molecular targets.We thoroughly analyze the mechanisms by which MQC-mediated exercise can improve the skeletal muscle atrophy caused by aging,disuse,and cancer cachexia in order to provide theoretical guidance for intervention.

Objective To investigate the differences of curriculum designs for undergraduate nursing majors among different TCM colleges and universities;To provide evidence for the development of the accreditation standards for academic quality of baccalaureate degree program in TCM colleges and universities which can be used as the standards for teaching reform. Methods Cultivating plans of 20 TCM colleges and universities for undergraduate nursing majors were collected. Current status and deficiency in curriculum design were obtained through comparative study and statistical analysis.Results The course names were lack of standardization;proportion of Chinese and Western medicine related courses were unreasonable;theoretical and practice teaching were irrelevant;optional courses were greatly inconsistent and irrational. Conclusion The further reform of the curriculum design for the undergraduate nursing majors in TCM colleges and universities is in urgent need, which can be standardized by developing the accreditation standards for academic quality of baccalaureate degree program in universities of Chinese Medicine.

OBJECTIVETo study the effect of cholecystokinin octapeptide (CCK-8) on lipopolysaccharide (LPS)-stimulated pulmonary interstitial macrophages (PIM) in vitro.

METHODSPIM were isolated and cultured in the presence or absence of LPS, CCK-8, proglumide (the antagonist of CCK receptors) and vehicle. The expression of membrane CD14 (mCD14) protein was assayed by flow cytometry and soluble CD14 (sCD14) in the supernatant was analyzed semi-quantitatively by Western blot. TNF-alpha in the supernatant was detected with ELISA.

RESULTSCCK-8, at concentrations of 10(-7) mol/L and 10(-6) mol/L, significantly inhibited the expression of mCD14. Release of sCD14 and TNF-alpha in the supernatant was up-regulated by LPS (1 microg/ml) but reduced by CCK-8. The effect of CCK-8 was inhibited by proglumide.

CONCLUSIONCCK-8 negatively modulated several functions of LPS-stimulated PIM through CCK receptors. This may be one of the mechanisms for CCK-8 to alleviate inflammation in lung tissue during endotoxemia.

Animals ; Cells, Cultured ; Culture Media, Conditioned ; chemistry ; Female ; Lipopolysaccharide Receptors ; biosynthesis ; Lipopolysaccharides ; pharmacology ; Macrophages, Alveolar ; cytology ; drug effects ; metabolism ; Rats ; Rats, Sprague-Dawley ; Sincalide ; pharmacology ; Specific Pathogen-Free Organisms ; Tumor Necrosis Factor-alpha ; drug effects ; secretion

Objective To construct a cDNA library of three-year old Polygonum multiflorum leaf tissues so as to further research the gene regulation of secondary metabolite biosynthesis of medicinal plants. Methods Total RNA from leaf tissues of P.multiflorum was extracted and mRNA was purified,which were synthesized to double strand cDNA through reverse transcription.After the cDNA termini was blunted,the 5' end of EcoR Ⅰ adapters phosphorylated was conjoined,and then digested by Xho Ⅰ,cDNA fragments were fractionated by Sepharose CL-2B spin column.The fragments longer than 400 bp were linked to Uni-ZAP XR vector.The primary cDNA library was established after the recombinants had been packaged.Uni-ZAP XR Vector might fleetly release pBluescript SK-phasmids at the presence of ExAssist helper phage of coinfection and inverted E.coli SOLR.Finally,PCR and double enzymes digestion were used to analyze the range of inserts,respectively. Results The titer of cDNA primary library was 1.07?106pfu/mL and the length of exogenous insert was at about 0.5-2.0 kb with 5.4?105 recombinants,the recombinants of amplified library were 4.25?1011 and the rate of recombination was 98.5%. Conclusion The results indicate that the cDNA library of P.multiflorum leaf tissues has enough volume for screening the desired genes and sets up a basis for studying on gene regulation of secondary metabolite biosynthesis of medicinal plants besides.

AIM:To observe the effects of cholecystokinin octapeptide(CCK-8) on the expression of proinflammatory cytokines IL-1?,IL-6 and anti-inflammatory cytokines IL-10,IL-4 in LPS-attacked mice.METHODS: Kunming mice were randomly assigned and injected intraperitoneally with LPS alone or/and CCK-8 at different time points.The expression of IL-1?,IL-6,IL-10 and IL-4 in the serum and lung tissues were assayed by ELISA and RT-PCR.RESULTS: The expression of IL-1?,IL-6,IL-10 and IL-4 were upregulated in LPS-attacked mice.Pre-treatment of CCK-8 decreased both IL-1? and IL-6 expression and augmented IL-10 and IL-4 expression in LPS-attacked mice.CONCLUSIONS: CCK-8 exerts an anti-inflammatory effect by inhibiting the expression of IL-1?,IL-6 and increasing the expression of IL-10,IL-4 in LPS-attacked mice,which could alleviate the inflammatory response in lung tissue.