With the process of China’s aging population intensifying， palliative care， as an important guarantee for improving the quality of life of terminally ill patients， is receiving more and more social attention， and the demand is constantly increasing. Palliative care needs versatile professionals， and general education can enhance people’s awareness and understanding of it， enabling more people to understand， accept， and participate in palliative care. With the advancement of knowledge and technology in palliative care， the traditional cramming education models are no longer able to meet the actual needs. Therefore， there is an urgent need to innovate palliative care education strategies. By analyzing the current problems in the general education of palliative care in China， this paper proposed thoughts and suggestions for general and innovative education of palliative care in several aspects， such as establishing general and innovative education systems and evaluation systems of palliative care， diversifying educational contents and methods， strengthening medical staffs training， promoting diversified student groups， and strengthening the popularization of palliative care knowledge among the public.

Objective To investigate the mechanism by which Erastin affects ferroptosis in lung fibroblasts.Meth-ods Mouse lung fibroblasts (C57/B6-L) were treated with varying concentrations of the iron death inducer Eras-tin.Cell viability was assessed using the cell counting Kit-8 (CCK-8) assay.Oxidative stress levels were visualized using a fluorescence microscope, and the expression of proteins related to the mitogen-activated protein kinase (MAPK) signaling pathway was analyzed using Western blot.Additionally, the p38 and extracellular regulated protein kinase (ERK) inhibitors SB203580 and U0126 were employed to further elucidate the mechanism by which Erastin induces iron death in lung fibroblasts.Results At a concentration of 100 μmol/L, Erastin effectively in-duced ferroptosis in lung fibroblasts, leading to an upregulation of oxidative stress.Furthermore, the phosphoryla-tion levels of p38 and ERK proteins in the MAPK pathway were elevated (P<0.05) .The addition of SB203580 and U0126 inhibitors resulted in a significant reduction in oxidative stress levels and a notable increased in cell ac-tivity in lung fibroblasts (P<0.05).Conclusion It can be concluded that Erastin induces ferroptosis in lung fi-broblasts, potentially through the mediation of oxidative stress via the MAPK signaling pathway.

Objective To explore the therapeutic mechanism of maggot for psoriasis-like lesions in mice from the perspective of immune stress and complement activation regulation.Methods Thirty-six male C57BL/6 mice were randomly divided into control group,model group,maggot(1.25%,2.5%,and 5%)groups,and Benvitimod(1%)group.Psoriasis-like lesions were induced by application of imiquimod cream,and the severity of skin lesions was assessed using the modified Psoriasis Area and Severity Index(MPASI)score.Auricular swelling of the mice was observed,and histopathological changes of the skin lesions were examined with HE staining.Scratching behavior of the mice was observed and the spleen index was calculated.Toluidine blue staining was used to detect mast cells in the skin lesions,and serum levels of IgG,IgM,the complements CH50,C1s,C3,C3a,C5 and C5a,and the inflammatory factors IL-23,IL-17A and TNF-α were determined with ELISA.Results In mice with imiquimod-induced psoriasis-like skin lesions,treatment with the maggot at the 3 doses significantly decreased MPASI score,alleviated auricular swelling and pathologies in the skin lesions,reduced scratching behaviors,spleen index,and the number of mast cells in the lesions.Treatment with high-dose maggot significantly lowered serum levels of IgG,C1s,C3a,C5a,IL-23,IL-17A and TNF-α and the levels of C1s,C3,C3a,C5 and C5a in the lesion tissue,and increased serum levels of CH50,C3,and C5.The therapeutic effect of maggot showed a dose-effect dependence.Conclusion Maggot can alleviate psoriasis-like skin lesions in mice by inhibiting immune stress and complement activation.

Objective To explore the therapeutic mechanism of maggot for psoriasis-like lesions in mice from the perspective of immune stress and complement activation regulation.Methods Thirty-six male C57BL/6 mice were randomly divided into control group,model group,maggot(1.25%,2.5%,and 5%)groups,and Benvitimod(1%)group.Psoriasis-like lesions were induced by application of imiquimod cream,and the severity of skin lesions was assessed using the modified Psoriasis Area and Severity Index(MPASI)score.Auricular swelling of the mice was observed,and histopathological changes of the skin lesions were examined with HE staining.Scratching behavior of the mice was observed and the spleen index was calculated.Toluidine blue staining was used to detect mast cells in the skin lesions,and serum levels of IgG,IgM,the complements CH50,C1s,C3,C3a,C5 and C5a,and the inflammatory factors IL-23,IL-17A and TNF-α were determined with ELISA.Results In mice with imiquimod-induced psoriasis-like skin lesions,treatment with the maggot at the 3 doses significantly decreased MPASI score,alleviated auricular swelling and pathologies in the skin lesions,reduced scratching behaviors,spleen index,and the number of mast cells in the lesions.Treatment with high-dose maggot significantly lowered serum levels of IgG,C1s,C3a,C5a,IL-23,IL-17A and TNF-α and the levels of C1s,C3,C3a,C5 and C5a in the lesion tissue,and increased serum levels of CH50,C3,and C5.The therapeutic effect of maggot showed a dose-effect dependence.Conclusion Maggot can alleviate psoriasis-like skin lesions in mice by inhibiting immune stress and complement activation.

Objective:To summarize the clinical features of epilepsy and (or) developmental delay associated with KCNB1 gene variants in children.Methods:A case series study was conducted on 24 children with KCNB1 gene variants associated with epilepsy and (or) developmental delay who were treated at the Children′s Medical Center of Peking University First Hospital and the Department of Neurology of Shenzhen Children′s Hospital from July 2015 to June 2024. The manifestations of seizures, electroencephalogram (EEG) and genetic test results of those children were analyzed.Results:All the KCNB1 gene variants were de novo, involving 20 different variation, including 15 missense variations, 3 frameshift variations and 2 nonsense variations. There were 7 novel variations. Among the 24 developmental and epileptic encephalopathy children, there were 14 boys and 10 girls. The last follow-up age ranged from 9 months to 13 years and 9 months. Seizures were present in 21 children (88%), with onset ranging from 1 month to 7 years, and 76% (16/21) began before 2 years of age. The seizure types included focal seizures in 15 children (71%), epileptic spasms, myoclonic seizures, and generalized tonic-clonic seizures in 6 children respectively, atypical absence seizures in 4 children, and myoclonic atonic seizures in 1 child. Seventeen children (81%) had a cluster of seizures and 5 had a history of focal status epilepticus with impaired consciousness. All 24 children had varying degrees of developmental delay, with 3 presenting solely developmental delay. EEG abnormalities were present in all the 21 children with seizures, including focal or multifocal discharges in 20 children, generalized discharges in 10 children, hypsarrhythmia in 2 children, and electrical status epilepticus during sleep in 3 children. Magnetic resonance imaging abnormalities were found in 5 of the 24 children. Among the 21 children with seizures, 57% (12/21) achieved seizure control.Conclusions:KCNB1 gene variants are predominantly de novo missense variation. Most affected children present with epilepsy, though some may exhibit only developmental delay. Epilepsy often begins before 2 years of age, with focal seizures being the most common type. About 80% of patients experience clustered seizures. Although most patients achieve seizure control, they still exhibit varying degrees of developmental delay, consistent with developmental epileptic encephalopathy.

OBJECTIVE: To explore the regulatory mechanism of human hepatocyte apoptosis induced by lysosomal membrane protein Sidt2 knockout. METHODS: The Sidt2 knockout (Sidt2^-/-) cell model was constructed in human hepatocyte HL7702 cells using Crispr-Cas9 technology.The protein levels of Sidt2 and key autophagy proteins LC3-II/I and P62 in the cell model were detected using Western blotting, and the formation of autophagosomes was observed with MDC staining.EdU incorporation assay and flow cytometry were performed to observe the effect of Sidt2 knockout on cell proliferation and apoptosis.The effect of chloroquine at the saturating concentration on autophagic flux, proliferation and apoptosis of Sidt2 knockout cells were observed. RESULTS: Sidt2^-/- HL7702 cells were successfully constructed.Sidt2 knockout significantly inhibited the proliferation and increased apoptosis of the cells, causing also increased protein expressions of LC3-II/I and P62(P < 0.05) and increased number of autophagosomes.Autophagy of the cells reached a saturated state following treatment with 50 μmol/L chloroquine, and at this concentration, chloroquine significantly increased the expressions of LC3B and P62 in Sidt2^-/- HL7702 cells. CONCLUSION Sidt2 gene knockout causes dysregulation of the autophagy pathway and induces apoptosis of HL7702 cells, and the latter effect is not mediated by inhibiting the autophagy-lysosomal pathway.
Humans ; Lysosome-Associated Membrane Glycoproteins/metabolism* ; Autophagy ; Apoptosis ; Hepatocytes ; Lysosomes/metabolism* ; Chloroquine/pharmacology* ; Nucleotide Transport Proteins/metabolism*

Objective:To investigate the clinical efficacy of redo rectal resection and coloanal anastomosis.Methods:The retrospective and descriptive study was conducted. The clinicopatholo-gical data of 49 patients who underwent redo rectal resection and coloanal anastomosis for the treatment of local recurrence of tumors and failure of colorectal or coloanal anastomosis after rectal resection in the Sixth Affiliated Hospital of Sun Yat-sen University from November 2012 to December 2021 were collected. There were 32 males and 17 females, aged 57(range,31-87)years. Redo rectal resection and coloanal anastomosis was performed according to the patient′s situations. Observa-tion indicators: (1) surgical situations; (2) postoperative situations; (3) follow-up. Measurement data with normal distribution were represented as Mean± SD, and measurement data with skewed distri-bution were represented as M( Q1, Q3) or M(range). Count data were described as absolute numbers or percentages. Results:(1) Surgical situations. All 49 patients underwent redo rectal resection and coloanal anastomosis successfully, with the interval between the initial surgery and the reopera-tion as 14.2(7.1,24.3)months. The operation time and volume of intraoperative bold loss of 49 patients in the redo rectal resection and coloanal anastomosis was 313(251,398)minutes and 125(50,400)mL, respectively. Of the 49 patients, there were 38 cases receiving laparoscopic surgery including 12 cases with transanoscopic laparoscopic assisted surgery, 11 cases receiving open surgery including 2 cases as conversion to open surgery, there were 20 cases undergoing Bacon surgery, 14 cases undergoing Dixon surgery, 12 cases undergoing Parks surgery, 2 cases undergoing intersphincter resection and 1 case undergoing Kraske surgery, there were 20 cases undergoing rectum dragging out excision and secondary colonic anastomosis, 13 cases undergoing dragging out excision single anastomosis, 12 cases undergoing rectum dragging out excision double anastomosis, 4 cases undergoing first-stage manual anastomosis, there were 21 cases with enterostomy before surgery, 16 cases with prophylactic enterostomy after surgery, 12 cases without prophylactic enterostomy after surgery. The duration of postoperative hospital stay of 49 patients was (14±7)days. (2) Postoperative situations. Fifteen of 49 patients underwent postoperative complications, including 8 cases with grade Ⅱ Clevien-Dindo complications and 7 cases with ≥grade Ⅲ Clevien-Dindo complications. None of 49 patient underwent postoperative transferring to intensive care unit and no patient died during hospitalization. Results of postoperative histopathological examination in 23 patients with tumor local recurrence showed negative incision margin of the surgical specimen. (3) Follow-up. All 49 patients underwent post-operative follow-up of 90 days. There were 42 cases undergoing redo rectal resection and coloanal anastomosis successfully and 7 cases failed. Of the 37 patients with enterostomy, 20 cases failed in closing fistula, and 17 cases succeed. There were 46 patients receiving follow-up with the median time as 16.1(7.5,34.6)months. The questionnaire response rate for low anterior resection syndrome (LARS) score was 48.3%(14/29). Of the patients who underwent redo coloanal anastomosis and closure of stoma successfully, there were 9 cases with mild-to-moderate LARS.Conclusion:Redo rectal resection and coloanal anastomosis is safe and feasible for patients undergoing local recurr-ence of tumors and failure of colorectal or coloanal anastomosis after rectal resection, which can successfully restore intestinal continuity in patients and avoid permanent enterostomy.

Objective:Continuous glucose monitoring (CGM) technology is used to compare the advantages of insulin degludec (IDeg) as a basal insulin regimen compared with insulin glargine (IGlar) in the treatment of adult type 1 diabetes mellitus.Methods:30 adult patients with T1DM admitted to Heji Hospital Affiliated to Changzhi Medical College from September 2019 to December 2020 were screened. According to the random number table method, the patients were randomly divided into two groups (insulin degludec group and insulin glargine group) at a ratio of 1∶1, respectively treated with IDeg, IGlar and aspartate insulin for 12 weeks. The main outcome measures were the coefficient of variation of blood glucose (CV), mean amplitude of glycemic excursions (MAGE), time in range (TIR), time above range (TAR) and time below range (TBR). The secondary outcome measures were mean blood glucose (MBG), standard deviation of blood glucose (SD), fasting blood glucose (FPG), 2 h postprandial blood glucose (2 h BG), hemoglobin A1c (HbA 1c), means of daily differences (MOOD), and the frequency of hypoglycemic events. Results:At 12 weeks of treatment, the HbA 1c, FPG, 2 h BG, MBG, SD, CV and MAGE of insulin degludec group were lower than those of insulin glargine group, with statistically significant difference (all P<0.05). The TIR in the insulin degludec group was significantly higher than that in the insulin glargine group [73(63, 75)% vs 43(28, 63)%, P<0.001], and the TAR was lower than that in the glycerine group [25(17, 23)% vs 35(33, 64)%, P=0.003]. From the curve spectrum of blood glucose level of the two groups, the stability of blood glucose in the insulin degludec group was better than that in the insulin glargine group. After 12 weeks of treatment, 8 cases (8/15) in insulin degludec group had HbA 1c<7.0%, and 4 cases (4/15) in insulin glargine group had HbA 1c<7.0%, without statistically significant difference ( P=0.264). There were 7 cases (7/15) in the insulin degludec group and 1 case (1/15) in the insulin glargine group who achieved high quality blood glucose control, with statistically significant difference ( P=0.035). At the 12th week of outpatient follow-up, the incidence of nocturnal hypoglycemic events in insulin degludec group was significantly lower than that in insulin glargine group (4/15 vs 11/15, P=0.027). Conclusions:Compared with insulin glargine, insulin degludec can achieve higher blood glucose compliance rate, lower blood glucose level and reduce blood glucose fluctuations in patients with type 1 diabetes.

Objective:To explore the expression of long non-coding RNA (lncRNA) HAGLR in breast cancer and its effect on the prognosis of breast cancer, and to construct a competitive endogenous RNA (ceRNA) network.Methods:The Atlas of Genetics and Cytogenetics in Oncology and Haematology website was used to search for HAGLR chromosome gene mapping and transcript expression. The lnclocater website was used to predict the subcellular localization of HAGLR, and the differential expression of HAGLR in breast cancer tissues and adjacent tissues was analyzed by using lnCAR database. The patients in lnCAR database were divided into HAGLR high expression group and HAGLR low expression according to HAGLR expression. The Kaplan-Meier method was used to analyze the overall survival (OS) and metastasis-free survival, which was verified by using UCSC Xena database. lnCAR database was used to search the co-expressed genes of HAGLR. The top 200 co-expressed genes were submitted to the Metascape website for Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) functional enrichment analysis, and protein interaction network (PPI) was constructed. Starbase, a bioinformatics online analysis website, was used to predict HAGLR targeting mircoRNA (miRNA) and mRNA that directly encoded proteins. ceRNA network of HAGLR was constructed with Cytoscape3.8 software.Results:HAGLR gene was localized in 2q31.1 and mainly distributed in cytoplasm. The expression level of HAGLR in breast cancer tissues was higher than that in adjacent tissues, and the difference was statistically significant ( P < 0.001). lnCAR database and UCSC Xena database analysis showed that OS in HAGLR high expression group was worse than that in HAGLR low expression group (all P < 0.01). lnCAR database, the metastasis-free survival in HAGLR high expression group was worse than that in HAGLR low expression group ( P = 0.030). Among the top 200 HAGLR co-expressed genes, 129 genes were negatively correlated with HAGLR and 71 genes were positively correlated with HAGLR. KEGG pathway analysis showed that HAGLR was related to metabolic pathways, MAPK signaling pathway, JAK-STAT signaling pathway and cancer pathway. GO annotation analysis showed that HAGLR was mainly enriched in cell cycle, centromeric complex assembly, mitotic progression, protein kinase binding, kinase activity regulation, cell response to DNA damage stimulation and other functions. hsa-miR-130b-3p, hsa-miR-1245b-5p, hsa-miR-182b-5p, hsa-miR-512-3p, hsa-miR-302b-3p, hsa-miR-185b-5p, hsa-miR-106b-5p were HAGLR targeting miRNA. Conclusions:HAGLR is highly expressed in breast cancer tissues, and it may be a biomarker for predicting the prognosis of breast cancer.

Objective To evaluate the methodological quality and measurement characteristics of health literacy assessment tools for diabetic patients and to provide references for medical staff to select the best assessment tools.Methods The PubMed,Embase,CINAHL,Web of Science,CNKI,VIP database,Wanfang Data,and Chinese Biomedical Database were searched from inception to December 31,2022.Data were screened and extracted independently by 2 researchers.The consensus-based standards for the selection of health measurement instruments(COSMIN)system evaluation guidelines were spontaneously used to evaluate the included assessment tools.Finally,recommendations were made.Results A total of 15 studies were included,involving 12 health literacy assessment tools for diabetic patients.Among them,KHLS-DM and DNT-15 have satisfactory content validity and internal consistency and are recommended as Grade A.HLSQ-3 has high-quality evidence to suggest that its internal consistency is"inadequate"and recommended as Grade C,while the other 9 scales are recommended as Grade B for content validity or internal consistency of uncertain/inadequate evidence at or above the intermediate level.Conclusion KHLS-DM can evaluate written literacy,numeracy,and critical literacy of patients,and each measurement characteristic has been comprehensively evaluated with high reliability and validity,so it is recommended to be applied first.DNT-15 focuses on evaluating the numeracy of patients,which can be used in combination with other scales to evaluate health literacy of patients more comprehensively.