Social robots play an important role in the field of medical companionship， providing services such as companion communication， drug monitoring， and rehabilitation guidance for the elderly and other subjects. However， social robots also pose the risk of deceiving medical users. Although certain forms of social robots’ deception can be used for therapeutic purposes， unethical deception can have adverse consequences for patients， doctors， and even society. These risks include causing patients to develop attachment disorders， violating their privacy， endangering their health， and even undermining the credibility of the healthcare system. Faced with the deception problem of social robots， starting from relational theory， medical artificial intelligence developers can conduct ethical regulation from the following two paths. First， social robots should be ethically programmed， including embedding programs for limiting benevolent lies， implementing informed consent principles， and ensuring information accuracy. Second， the deceptive behaviors of social robots should be controlled， requiring developers to take full-process supervision responsibility， design medical social robots that can supervise each other， and participate in formulating quality standards and evidence mechanisms for deception issues.

Post-stroke urinary incontinence (PSUI) is a common complication in patients with stroke, affecting at least one-third of patients with stroke and seriously affecting their quality of life and rehabilitation process. This article reviews the pathogenesis, risk factors, and treatment of PSUI.

Bluetongue virus is an arbovirus that seriously harms ruminants such as sheep,this study aims to investigate the molecular mechanism of bluetongue virus infection and host cell interferon antiviral immune response.The study was conducted to characterize the mRNA expression of inter-feron pathway genes by real-time fluorescence quantitative PCR,as well as Western blot analysis of MDA5,TRAF3,RIG-Ⅰ,and TBK1 protein expression in BHK-21 cells induced by BTV with a multiplicity of infections(MOI)of 1 for 18,24,and 36 h.The results showed that the most pro-nounced changes in the expression of interferon signaling pathway genes were observed at 24 h of induction,the gene mRNA expression levels of the IFN-α,IFN-β,RIG-Ⅰ,TBK1,MDA5,VISA,and TRAF3 genes were upregulated.However,the mRNA expression levels of IKKε and TRAF6 genes were downregulated.At the protein level,MDA5 and TBK1 proteins were upregulated while RIG-1 and TRAF3 proteins were downregulated,which showed that BTV infection induces a typeⅠ interferon immune response in BHK-21 cells.This study lays the foundation for further exploring the antiviral immunity mechanism of IFN-Ⅰ signaling pathway regulatory genes in host cells infected with BTV infection.

Pyroptosis is a programmed death of inflammatory cells triggered by pathogen invasion,dependent on caspase activation,through both classical and non-classical pyroptosis pathways.Cell pyroptosis is related to the occurrence and development of a variety of animal infectious diseases caused by microbial infection.After microorganisms invading,cells are stimulated by pathology-re-lated molecular patterns,causing strong immune response,stimulating inflammatory signaling pathways,and then activating inflammasome,leading to pyroptosis.The immune system has e-volved multiple mechanisms to fight microbial infections and regulate inflammatory responses.The innate immune system,by recognizing microbial molecules in pathogens and responding quickly by producing inflammasome and activating pyroptosis,helps clear pathogens to prevent infection and maintain the normal functioning of the body.A thorough study of the pathogenesis and immune es-cape mechanism of cell pyroptosis in animal infectious diseases will provide a new direction for the treatment of animal infectious diseases.

Objective To investigate the involvement of calmodulin(CaM)in the pathogenesis of Alzheimer disease(AD)and the mechanism by which CaM binds to amyloid-β(Aβ).Methods The hub genes expressed in AD and predicted to be the target proteins for AD prevention and treatment were obtained using bioinformatics methods.The GST-Aβ1-42 recombinant plasmid was constructed through genetic recombination and was then sequenced.The recombinant plasmids were identified using agarose gel electrophoresis,while the extracted and purified GST-Aβ1-42 fusion protein was confirmed using SDS-PAGE gel electrophoresis.GST pull-down assay was used to detect the interaction between GST-Aβ1-42 protein and CaM,expressed in the plasmid.Results The top 20 hub genes in degree ranking were obtained.The DNA sequencing results of the plasmid proved that the recombinant plasmid was successfully constructed.The agarose gel electrophoresis results indicated that the fragment digested by the enzyme was similar to the molecular weight of the Aβ1-42 gene seg-ments,further proving the successful construction of the recombinant plasmid.Binding of GST-Aβ1-42 protein to CaM in a concentration dependent manner was revealed through the GST pull down experiment.Conclusion The GST-Aβ1-42 recombinant plasmid is success-fully constructed and is shown to bind to CaM.

Objective To find out the willingness to choose old-age care mode and the influencing factors of the elderly in the younger age group.Methods A multi-stage stratified whole cluster random sampling method was used to conduct a questionnaire survey on the willingness of the younger elderly in Zhangye City.Results The proportion of low-aged elderly in Zhangye City who chose family old-age care was the highest,and factors such as who they relied on to solve their old-age problems,opinions on moving into old-age care institutions,knowledge of the combination of medical care and nursing care,loneliness,and the number of chronic illnesses affected the willingness of low-aged elderly to live in old-age care.Conclusion In Zhangye City,family care is the main mode of old-age care for low-aged elderly.In the future,the relevant government departments should take into account the diversified needs of the elderly and the characteristics of the influencing factors,in order to realise the precise supply of the demand for elderly care services for the elderly.

Objective To explore the corneal wound healing mechanism after 3.74 μm infrared laser irradiation.Methods Twenty-seven C57BL/6J mice(six to eight weeks old)were randomly divided into a normal group(3 mice)and an experimental group(24 mice).Mice in the normal group were not subjected to any treatment.The corneas of mice in the experimental group were damaged by infrared laser at a wavelength of 3.74 μm.The spot diameter was 2 mm,the exposure duration 0.8 s,and the radiant exposure 23.2 J·cm-2.Pathological sectioning of corneas was performed at 3 h,6 h,12 h,1 d,3 d,7 d,14 d,and 21 d after laser irradiation in the experimental group,with 3 mice at each time point.It was the same for mice in the normal group.Immunohistochemical staining was conducted to examine neutrophil elastase,CD68,CD163 and thrombomodulin-positive cells and identify neovascularization.Results Neutrophil elastase,CD68,CD163,and thrombomodulin-positive cells were not detected in the corneal stroma of mice in the normal group.Neutrophil elastase-positive cells were detected in the damaged corneal periphery of mice in the experimental group at 3 h,migrated to the damaged area at 12 h,peaked at 1 d,and then decreased gradually with time,but still existed slightly at 21 d after laser irradiation.CD68-positive cells were detected in the damaged corneal periphery of mice in the experimental group at 12 h and in the damaged area at 1 d through 21 d after laser irradiation.CD163-positive cells were found in the damaged corneal periphery of mice in the experimental group at 7 d and in the damaged area at 14 d and 21 d after laser irradiation.Throm-bomodulin-positive cells were found in the damaged area of the corneal stroma at 14 d and 21 d after laser irradiation.Con-clusion During the wound healing process after 3.74 μm infrared laser-induced full-thickness corneal injury in mice,a large number of inflammatory cells migrate from the damaged corneal periphery or limbus to the damaged area.Neutrophils and M1 macrophages infiltrate in the early stage,while M2 macrophages are involved in the later stage,accompanied by neovascularization.

Objective To construct a carbon dioxide(CO2)laser-induced corneal injury model in mice and observe the process of corneal wound healing.Methods Twenty eyes of ten C57BL/6J mice were divided into 4 groups.The cen-tral corneas in each group were irradiated by CO2 laser with a wavelength of 10.6 μm,spot diameter of 2 mm and power of 0.94 W.The exposure doses were 3.0 J·cm-2,4.5 J·cm-2,7.5 J·cm-2 and 10.5 J·cm-2,with corresponding expo-sure durations of 0.10 s,0.15 s,0.25 s and 0.35 s.Corneal injury severity was assessed using a slit lamp microscope,opti-cal coherence tomography and histopathological evaluation at 1 day after the exposure to determine the proper exposure dose for constructing a corneal injury model.Subsequently,the corneal injury model was constructed and the same meth-ods were used to monitor wound healing before,and 0 hours to 6 months after the exposure.Results No obvious corne-al injury was observed at an exposure dose of 3.0 J·cm-2.At an exposure dose of 4.5 J·cm-2,an off-white injury area appeared on the central cornea with loss of epithelium and endothelium.At an exposure dose of 7.5 J·cm-2 or 10.5 J·cm-2,the injury area became porcelain white,the cornea was thickened,and the iris was seen adhering to the margin of the cornea.Therefore,4.5 J·cm-2 CO2 laser was selected to construct a corneal injury model.At this exposure dose,the cornea swelled and thickened rapidly after injury,reached the maximum thickness 1 day after the exposure,and then grad-ually recovered,returning to normal by 14 days after the exposure.In the early stage(0 hours to 3 days after the expo-sure),the cornea showed shedding of injured epithelium and endothelium,migration of new epithelium and endothelium,and infiltration and regression of inflammatory cells.At the late stage(7 days to 6 months after the exposure),the cornea gradually returned to a normal physiological state,but some of the injured cornea exhibited stromal hyperplasia.Conclu-sion A CO2 laser with an exposure dose of 4.5 J·cm-2 can be used to construct a corneal injury model in mice.The a-cute phase of corneal injury primarily occurs within 3 days after the exposure.The cornea tends to restore its original physi-ological structure,but the corneal transparency cannot return to a normal state.

Objective To observe the effects of Huoxue Digui Decoction on iron accumulation and ferroptosis in renal podocytes of diabetic nephropathy(DN)mice.Methods Totally 50 C57BL/6J mice were randomly divided into normal group(6 mice)and modeling group(44 mice).The DN model was established by streptozotocin injection.Mice conforming to DN model were randomly divided into model group(8 mice),and sulforaphane group,Huoxue Digui Decoction low-,medium-and high-dosage groups(6 mice for each group).The sulforaphane group was injected with sulforaphane intraperitoneally,while Huoxue Digui Decoction low-,medium-and high-dosage groups were orally administered with corresponding solution for 12 consecutive weeks.The fasting blood glucose,blood urea nitrogen,serum creatinine,24 h urinary albumin were detected,HE staining was used to observe the morphology of renal tissue,PAS staining was used to observe glycogen deposition in renal tissue,Masson staining was used to observe fibrosis in renal tissue;transmission electron microscopy was used to observe the ultrastructure of renal tissue,immunohistochemistry was used to detect the expressions of Podocin and Nephrin in renal tissue,Western blot was used to detect the protein expressions of glutathione peroxidase 4(GPX4),ACSL4,nuclear factor E2 related factor 2(Nrf2)and ferroportin 1(FPN1)in renal tissue,Prussian blue staining was used to observe the deposition of ferric ion in renal tissue.Results Compared with the normal group,the fasting blood glucose,blood urea nitrogen,serum creatinine and 24 h urinary albumin in model group significantly increased(P<0.01),with renal tissue capillary atrophy,increased glycogen deposition,and worsening fibrosis,the expressions of Podocin and Nephrin in renal tissue were down-regulated,while the expressions of GPX4,Nrf2 and FPN1 protein were significantly decreased(P<0.01),the expression of ACSL4 protein significantly increased(P<0.01),and the deposition of ferric ion in renal tissue increased.Compared with the model group,the fasting blood glucose,blood urea nitrogen,serum creatinine and 24 h urinary albumin in sulforaphane group and Huoxue Digui Decoction groups were reduced to different degrees(P<0.05,P<0.01),renal tissue pathological damage was reduced to varying degrees,glycogen deposition was reduced,and fibrosis was alleviated,the expressions of Podocin and Nephrin in renal tissue were up-regulated,while the expressions of GPX4,Nrf2 and FPN1 protein significantly increased(P<0.01),the expression of ACSL4 protein significantly decreased(P<0.05,P<0.01),and the deposition of ferric ion in renal tissue was reduced.Conclusion Huoxue Digui Decoction can alleviate renal pathological injury,reduce blood glucose and delay the progression of DN mice.The mechanism may be related to regulating the expressions of Nrf2 and FPN1,inhibiting iron accumulation and ferroptosis in renal podocytes of DN mice.

Background Quartz dust cannot be degraded in the lungs, and inhalation of a large amount of quartz dust in the occupational production process will lead to the occurrence of pulmonary fibrosis, and then develop into silicosis. In recent years, studies have found that exosomes may be involved in the pathogenesis of fibrotic diseases by carrying microribonucleic acid (miRNA), but the mechanism of their actions in silicosis still needs to be studied. Objective To investigate the role of exosome-derived miRNA-21-5p/mothers against decapentaplegic homolog 7 (Smad7) in quartz dust-induced pulmonary fibrosis in rats. Methods Twenty-four healthy male SD rats were randomly divided into four groups (six rats in each group): control 4-week group, control 16-week group, quartz 4-week group, and quartz 16-week group. At the beginning of the experiment, 1 mL of quartz suspension (50 mg·mL⁻¹) and 1 mL of normal saline were injected into the trachea of rats in the quartz group and the control group, respectively, by means of one-time non-exposure intratracheal dust staining. Alveolar lavage was performed at the 4th and 16th weeks after dust staining, the exosomes in lavage solution were extracted by polyethylene glycol (PEG) precipitation, morphological identification was conducted by transmission electron microscopy (TEM), particle size of exosomes was detected by nano-tracking analysis (NTA), and the marker proteins CD9 and CD63 of exosomes were detected by Western blotting (WB). The expression of miRNA-21-5p in exosomes was determined by reverse transcription polymerase chain reaction (RT-PCR). The degree of lung tissue injury and fibrosis was observed by hematoxylin-eosin staining (HE) and Masson staining. The collagen content of lung tissue was detected by hydroxyproline (HYP) method. The expression of Smad7 protein in lung tissue was detected by WB. Results The results of pathological staining showed that compared with the control group, lung inflammatory cell infiltration, alveolar wall thickening, and collagen increase were observed after 4 weeks of dusting, and collagen deposition and silicon nodules appeared after 16 weeks of dusting. Compared with the control group, the expression level of HYP in the lung tissue of the quartz group was increased after 4 weeks and 16 weeks of dust staining (P<0.05). Transmission electron microscopy showed that exosomes were saucer-shaped, and the average particle size of exosomes was 95.8 nm by NTA. Positive expression of exosome marker proteins CD9 and CD81 was found by WB. Compared with the control group, the expression of exosome-derived miRNA-21-5p in alveolar lavage fluid in the quartz group increased in the 4th week and the 16th week (P<0.05), and the expression of Smad7 protein in lung tissue decreased (P<0.05). Conclusion Exosome-derived miRNA-21-5p and Smad7 may be involved in the mechanism of quartz dust-induced pulmonary fibrosis in rats.