Programmed cell death (PCD) is characterized as a cell death pathway governed by specific gene-encoding requirements, plays crucial roles in the homeostasis and innate immunity of organisms, and serves as both a pathogenic mechanism and a therapeutic target for a variety of human diseases. Z-DNA-binding protein 1 (ZBP1) functions as a cytosolic nucleic acid sensor, utilizing its unique Zα domains to detect endogenous or exogenous nucleic acids and its receptor-interacting protein homotypic interaction motif (RHIM) domains to sense or bind specific signaling molecules, thereby exerting regulatory effects on various forms of PCD. ZBP1 is involved in apoptosis, necroptosis, pyroptosis, and PANoptosis and interacts with molecules, such as receptor-interacting protein kinase 3 (RIPK3), to influence cell fate under various pathological conditions. It plays a crucial role in regulating PCD during infections, inflammatory and neurological diseases, cancers, and other conditions, affecting disease onset and progression. Targeting ZBP1-associated PCD may represent a viable therapeutic strategy for related pathological conditions. This review comprehensively summarizes the regulatory functions of ZBP1 in PCD and its interactions with several closely associated signaling molecules and delineates the diseases linked to ZBP1-mediated PCD, along with the potential therapeutic implications of ZBP1 in these contexts. Ongoing research on ZBP1 is being refined across various disease models, and these advancements may provide novel insights for studies focusing on PCD, potentially leading to new therapeutic options for related diseases.

In 1861, the missionary William Lockhart founded the Peking Hospital in Beijing. From 1861 to 1863, William Lockhart not only cured a large number of patients in the Peking Hospital but also introduced western surgical techniques, hygiene and disinfection concepts, and medical record management systems. During its operation, the Peking Hospital's unique value can be seen in its sources and modes of financing, scope of services, number of patients treated, and missionary functions. The Peking Hospital served as a vital bridge for the exchange of medical knowledge between the East and the West, and it played a pivotal role in transforming China's modern medical system and modern health concepts, exerting a profound influence on the development of modern medicine.

Diabetes mellitus is a metabolic disease characterized by chronic hyperglycemia caused by absolute or relative insufficiency of insulin secretion. As the disease progresses， patients begin to suffer from diabetic nephropathy， diabetic cardiomyopathy， non-alcoholic fatty liver disease or other complications， which increase the burden on the patients. Moreover， the number of patients is increasing， which brings a heavy burden to the society. Ferroptosis is a new type of programmed cell death which has attracted wide attention in recent years. It refers to the cell death caused by the excessive accumulation of lipid peroxide under the overload of iron ions. Studies have discovered that ferroptosis exists in diabetes mellitus and its complications. Inhibiting ferroptosis can greatly slow down the occurrence and progression of diabetes mellitus and its complications. Chinese medicine， the unique medical treasure in China， acts in a multi-pathway， multi-target manner and is praised for the cheap price， low toxicity， and mild side effects. It has been widely used in the treatment of diabetes mellitus and its complications and has demonstrated definite therapeutic effects， bringing the good news for the majority of patients. The regulation of ferroptosis by Chinese medicine may be a new direction for the treatment of diabetes mellitus and its complications in the future. This paper briefly describes the mechanism of ferroptosis， explores the relationship of ferroptosis with diabetes mellitus and its complications， summarizes the research status of Chinese medicine interventions， and puts forward suggestions， aiming to provide a reference for further research on the treatment of diabetes mellitus and its complications with Chinese medicine.

Objective This study aimed to investigate the effects of sitagliptin on the proliferation,apoptosis,in-flammation,and osteogenic differentiation of human periodontal ligament stem cells(hPDLSCs)in lipopolysaccharide(LPS)-induced inflammatory microenvironment and its molecular mechanism.Methods hPDLSCs were cultured in vitro and treated with different concentrations of sitagliptin to detect cell viability and subsequently determine the exper-imental concentration of sitagliptin.An hPDLSCs inflammation model was established after 24 h of stimulation with 1 μg/mL LPS and divided into blank,control,low-concentration sitagliptin(0.5 μmol/L),medium-concentration sita-gliptin(1 μmol/L),and high-concentration sitagliptin(2 μmol/L),high-concentrationsitagliptin+stromal cell derived factor-1(SDF-1)/CXC chemokine receptor 4(CXCR4)pathway inhibitor(AMD3100)(2 μmol/L+10 μg/mL)groups.A cell-counting kit-8 was used to detect the proliferation activity of hPDLSCs after 24,48,and 72 h culture.The apoptosis of hPDLSCs cultured for 72 h was detected by flow cytometry.After inducing osteogenic differentiation for 21 days,alizarin red staining was used to detect the osteogenic differentiation ability of hPDLSCs.The alkaline phosphatase(ALP)activity in hPDLSCs was determined using a kit.The levels of inflammatory factors[tumor necrosis factor(TNF)-α,interleukin(IL)-1β,and IL-6]in the supernatant of hPDLSCs culture were detected by enzyme-linked immu-nosorbent assay.The mRNA expressions of osteogenic differentiation genes[Runt-associated transcription factor 2(RUNX2),osteocalcin(OCN),osteopontin(OPN)],SDF-1 and CXCR4 in hPDLSCs were detected by real-time fluores-cence quantitative polymerase chain reaction(RT-qPCR).Western blot analysis was used to determine SDF-1 and CX-CR4 protein expression in hPDLSCs.Results Compared with the blank group,the proliferative activity,number of mineralized nodules,staining intensity,ALP activity,and RUNX2,OCN,OPN mRNA,SDF-1,and CXCR4 mRNA and protein expression levels of hPDLSCs in the control group significantly decreased.The apoptosis rate and levels of TNF-α,IL-1β,and IL-6 significantly increased(P<0.05).Compared with the control group,the proliferative activity,number of mineralized nodule,staining intensity,ALP activity,and RUNX2,OCN,OPN mRNA,SDF-1,and CXCR4 mRNA and protein expression levels of hPDLSCs in low-,medium-,and high-concentration sitagliptin groups in-creased.The apoptosis rate and levels of TNF-α,IL-1β,and IL-6 decreased(P<0.05).AMD3100 partially reversed the effect of high-concentration sitagliptin on LPS-induced hPDLSCs(P<0.05).Conclusion Sitagliptin may promote the proliferation and osteogenic differentiation of hPDLSCs in LPS-induced inflammatory microenvironment by activating the SDF-1/CXCR4 signaling pathway.Furthermore,it inhibited the apoptosis and inflammatory response of hPDLSCs.

Objective: To explore the changes in ribosomal DNA copy number in peripheral blood among patients with pneumoconiosis and its influencing factors, so as to provide insights into prevention and treatment of pneumoconiosis. Methods: Eighty-eight patients with pneumoconiosis who visited a designated hospital and 71 community residents with no history of pneumoconiosis or dust exposure were selected as the pneumoconiosis group and control group, and age, smoking history, drinking history and cumulative years of exposure to dust were collected through questionnaire surveys. The copy number of 45S rDNA and 5S rDNA was detected using real-time fluorescence quantitative PCR, and the differences between the two groups were compared. Factors affecting the copy number of 45S rDNA and 5S rDNA were identified by a multiple linear regression model. Results: The pneumoconiosis group had a median age of 56.00 (interquartile range, 15.25) and a mean cumulative dust exposure duration of (12.40±8.08) years, with 56.82% smoking and 62.50% drinking. The control group had a median age of 64.00 (interquartile range, 37.00) years, with 32.39% smoking and 26.76% drinking. The median copy number of 45S rDNA in the pneumoconiosis group was 1.29 (interquartile range, 0.59), which was lower than 2.10 (interquartile range, 1.88) in the control group; the median copy number of 5S rDNA in the pneumoconiosis group was 5.33 (interquartile range, 0.85), which was higher than 4.66 (1.34) in the control group (both P<0.05). Multiple linear regression analysis identified age (β=-0.034) and pneumoconiosis (β=-1.595) as factors affecting 45S rDNA copy number, age (β=-0.013) as a factor affecting 5S rDNA copy number, and age (β=0.018) as a factor affecting 5S rDNA copy number in the pneumoconiosis group (all P<0.05). Conclusions Compared with community residents with no history of pneumoconiosis or dust exposure, the copy number of 45S rDNA in peripheral blood among patients with pneumoconiosis is reduced and the copy number of 5S rDNA is increased.

Nonalcoholic fatty liver disease （NAFLD） is one of the most common complications of type 2 diabetes mellitus （T2DM）. Cell death caused by iron-lipid disorder is a new mode of regulating programmed cell death， which is characterized by lipid peroxidation induced by the accumulation of lipid reactive oxygen species and excessive accumulation of iron ions induced by iron metabolism disorders. Among them， iron homeostasis disorder and metabolic pathway disorder are the main causes of iron-lipid disorder， which play an important role in a variety of pathological processes related to cell death. Because the liver is an important organ for iron storage and lipid metabolism， iron-lipid disorder is an ideal target for liver disease， and inhibition of iron-lipid disorder may become a new strategy for the treatment of NAFLD. However， the pathogenic relationship and mechanism between NAFLD and iron-lipid disorder have not been fully elucidated. Based on the complex molecular regulation mechanism of iron-lipid disorder， by expounding the role of iron-lipid disorder in NAFLD and its related mechanism， this paper summarizes the research status of traditional Chinese medicine on the target treatment of NAFLD in recent years， so as to provide a new perspective and point out a new direction for the treatment of NAFLD in the future.

OBJECTIVE To investigate whether the microRNA-222(miRNA-222) carried by plasma exosomes can serve as an early warning marker for cognitive impairment induced by shRNA-PCSK9. METHODS The high-fat diet(HFD) was used to prepare a hypercholesterolemic mouse model group. The model group mice were divided into HFD-shRNA control group and HFD-shRNA-PCSK9 group. The shRNA-PCSK9 was constructed, injected intravenously into the body, and the expression of PCSK9 mRNA was detected by real-time PCR(RT-PCR). Tau protein and phosphorylation in brain tissue were observed by immunohistochemistry (IHC). Western blotting was used to detect Tau protein and P-Tau protein. Serum amyloid Aβ1-42Ab levels were determined by ELISA. The kits extracted plasma exosomes step by step, identify the exosome morphology by negative staining electron microscopy, and determined the size of exosomes by NTA technology. RT-PCR technique was used to detect the expression level of miRNA-222 carried in plasma exosomes. RESULTS The model mouse were prepared by feeding HFD for 13 weeks, whose total cholesterol(TC) and low-density lipoprotein(LDL-C) contents in serum were significantly increased. At the same time, the expression of PCSK9 mRNA in the brain tissue of model group was significantly increased. After shRNA-PCSK9 lentivirus interference, PCSK9 mRNA expression was inhibited, and IHC observed that shRNA-PCSK9 induced abnormal expression and hyperphosphorylation of Tau protein in brain tissue, indicating that the pathological changes of neurofibrillary tangles had occurred. However, at this time, serum Aβ1-42Ab had not been significantly increased, and it had not yet been of significance for the diagnosis of cognitive impairment. The miRNA in plasma exosomes was extracted, and RT-PCR results showed that the expression of miRNA-222 carried in the exosomes of the HFD-shRNA-PCSK9 group was significantly lower than that of the HFD-shRNA control group. CONCLUSION Plasma exosomes carried miRNA-222 provides an early warning marker for shRNA-PCSK9- induced cognitive impairment.

One of the most common and significant symptoms for skin disorders is pruritus.Additionally,it serves as a significant catalyst for the exacerbation or reoccurrence of skin diseases.Pruritus seriously affects patients'physical and mental health,and even the quality of life.It brings a heavy burden to the patients,the families,even the whole society.The pathogenesis and regulation mechanisms for pruritus are complicated and have not yet been elucidated.Previous clinical studies have shown that itch worsens at night in scabies,chronic pruritus,atopic dermatitis,and psoriasis,suggesting that skin pruritus may change with circadian rhythm.Cortisol,melatonin,core temperature,cytokines,and prostaglandins are the main regulatory factors of the circadian rhythm of pruritus.Recent studies have shown that some CLOCK genes,such as BMAL1,CLOCK,PER,and CRY,play an important role in the regulation of the circadian rhythm of pruritus by regulating the Janus tyrosine kinase(JAK)-signal transducer and activator of transcription(STAT)and nuclear factor kappa-B(NF-κB)signaling pathways.However,the mechanisms for circadian clock genes in regulation of circadian rhythm of pruritus have not been fully elucidated.Further studies on the mechanism of circadian clock genes in the regulation of circadian rhythm of pruritus will lay a foundation for elucidating the regulatory mechanisms for pruritus,and also provide new ideas for the control of pruritus and the alleviation of skin diseases.

Objective To establish a scientific training program that takes into account both anaerobic and aerobic training for pilots,and to explore the appropriate ratio of aerobic and anaerobic training.Methods According to the physical examination standards for pilots,a total of 16 healthy subjects aged 18-24 were selected from two batches.The two batches of subjects were trained with different aerobic and anaerobic ratios.Training period was 3 months.The changes in cardiopulmonary function of the subjects before and after training were evaluated using the cardiopulmonary function exercise testing system(CPET),and the changes in anaerobic capacity were evaluated using changes in strength as an indicator.Results After training,the weight load of the subjects in the two training programs,including barbell squats,leg flexion and hard pull,and barbell under 10RM and 3RM,was significantly increased(P<0.001),and there was no statistically significant difference in anaerobic strength growth between the two groups.The results of CPET showed that the maximum load,maximum heart rate,and respiratory quotient in the two groups were significantly increased after than before the training(P<0.01).The maximum load(Experiment group 1:29.12±19.69,Experiment group 2:72.00±46.24)and respiratory quotient(Experiment grouop 1:0.11±0.09,Experiment group 2:0.28±0.16)of the subjects in experiment group 2 before and after training were greater than those in experiment group 1.The difference was statistically significant(P<0.05).Conclusion The anaerobic and aerobic capacities of the subjects in the experiment group 2 are effectively improved,indicating that ratio of aerobic and anaerobic of the training scheme is better.

Objective:To search, evaluate and integrate the best evidence of the best evidence for emergency service surge capacity.Methods:According to the "6S" model of evidence resources, the related evidence on emergency service surge capacity in Guidelines International Network, National Guideline Clearinghouse, Canadian Medical Association CPG Infobase, Scottish Intercollegiate Guidelines Network, European Society for Emergency Medicine, the American College of Emergency Physicians, Emergency Nurses Association, Cochrane Library, PubMed, Embase, CINAHL, Web of Science, BMJ Best Practice, UpToDate,CKNI, Wanfang, and VIP database were searched by computer. The retrieval time limit was from the establishment of the database to Dec 31, 2023. Literature quality assessment and data extraction were performed by 2 researchers.Results:A total of 11 articles were included in this study, including 1 guideline, 7 expert consensuses and 3 systematic reviews, which summarized 43 pieces of evidence involving 7 categories, namely core elements, organizational management, space management, personnel allocation, material allocation, education and training, and support services.Conclusions:The best evidence summarized in this study can provide a reference for emergency service to improve surge capacity. In clinical application, emergency departments should focus on organizational, space, personnel and materials management, combined with the type of emergency events, to maximize their routine, emergency and crisis response capabilities, so as to respond to medical surges effectively.