ObjectiveTo explore the mechanisms associated with Mahoniae Caulis alkaloids （MA） in ameliorating depression by network pharmacology， molecular docking， and animal experiments. MethodsThe component targets of MA were obtained through Swiss Target Prediction and TCMIP database. The depression targets were collected through TCMIP， Genecards， HPO， DrugBank and OMIM database. The depression targets were collected through TCMIP， Genecards， HPO， DrugBank and OMIM database. Protein-protein interaction （PPI） network was constructed by protein interaction analysis （STRING） database. Gene ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） analyses were performed through Bioinformatics （DAVID） database. The docking of components and targets was performed by AGFR. The mouse model of depression was established by intraperitoneal injection of corticosterone （CORT） once a day for 35 consecutive days. Sixty mice were randomly allocated into control （0.9% normal saline）， model （CORT， 20 mg·kg^-1）， positive control （fluoxetine hydrochloride， 3.6 mg·kg^-1）， and MA （10， 5， and 2.5 mg·kg^-1） groups. Each group was administrated with corresponding medicine or normal saline once a day for 28 consecutive days. The depression-like behavior of mice was observed. The pathological changes of prefrontal cortex in mice were observed by hematoxylin-eosin staining. Terminal deoxynucleotidyl dUTP transferase nick end labeling （TUNEL） was employed to observe the apoptosis of neurons in the prefrontal cortex. Enzyme-linked immunosorbent assay was employed to assess the serum levels of brain-derived neurotrophic factor （BDNF）， dopamine （DA）， 5-hydroxytryptamine （5-HT）， and norepinephrine （NE） in mice. The mRNA levels of cyclic adenosine monophosphate （cAMP） pathway-related factors and inflammatory factors were determined by Real-time PCR. Western blot was employed to determine the expression of cAMP pathway-related factors and connexin 43 （Cx43）. ResultsA total of 434 component targets and 545 depression targets were obtained， including 84 common targets， among which 10 core targets were screened out. GO analysis predicted 34 biological processes， 15 cell components， and 11 molecular functions. The KEGG pathways were mainly related to gap junction and cAMP signaling pathway. The core components had good binding affinity with the core targets. The results of animal experiments showed that compared with the control group， CORT prolonged the immobility time of mice in forced swimming and tail suspension tests （P<0.01）， lowered the serum levels of NE， BDNF， and 5-HT （P<0.05）， up-regulated the mRNA levels of nuclear factor-κB （NF-κB） and interleukin-6 （IL-6） in the brain tissue （P<0.05）， and down-regulated the mRNA levels of cyclic adenosine monophosphate effector binding protein （CREB） and BDNF （P<0.05） and the protein levels of protein kinase （PRKACA）， phosphorylation （p）-CREB/CREB， BDNF， and Cx43 （P<0.05） in the brain tissue. Compared with the model group， high-dose MA reduced the immobility time of mice in forced swimming （P<0.05） and tail suspension （P<0.01） tests， raised the serum levels of NE， BDNF， and 5-HT （P<0.01）， down-regulated the mRNA level of NF-κB （P<0.01）， and up-regulated the mRNA level of BDNF （P<0.01） and protein levels of PRKACA， p-CREB/CREB， BDNF， and Cx43 （P<0.05）. ConclusionMA alleviates the CORT-induced depressive behavior of mice. It may play an antidepressant role by regulating cAMP signaling pathway and gap junction pathway， improving synaptic plasticity and gap junction function， and reducing neuroinflammation.

ObjectiveTo explore the mechanisms associated with Mahoniae Caulis alkaloids （MA） in ameliorating depression by network pharmacology， molecular docking， and animal experiments. MethodsThe component targets of MA were obtained through Swiss Target Prediction and TCMIP database. The depression targets were collected through TCMIP， Genecards， HPO， DrugBank and OMIM database. The depression targets were collected through TCMIP， Genecards， HPO， DrugBank and OMIM database. Protein-protein interaction （PPI） network was constructed by protein interaction analysis （STRING） database. Gene ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） analyses were performed through Bioinformatics （DAVID） database. The docking of components and targets was performed by AGFR. The mouse model of depression was established by intraperitoneal injection of corticosterone （CORT） once a day for 35 consecutive days. Sixty mice were randomly allocated into control （0.9% normal saline）， model （CORT， 20 mg·kg^-1）， positive control （fluoxetine hydrochloride， 3.6 mg·kg^-1）， and MA （10， 5， and 2.5 mg·kg^-1） groups. Each group was administrated with corresponding medicine or normal saline once a day for 28 consecutive days. The depression-like behavior of mice was observed. The pathological changes of prefrontal cortex in mice were observed by hematoxylin-eosin staining. Terminal deoxynucleotidyl dUTP transferase nick end labeling （TUNEL） was employed to observe the apoptosis of neurons in the prefrontal cortex. Enzyme-linked immunosorbent assay was employed to assess the serum levels of brain-derived neurotrophic factor （BDNF）， dopamine （DA）， 5-hydroxytryptamine （5-HT）， and norepinephrine （NE） in mice. The mRNA levels of cyclic adenosine monophosphate （cAMP） pathway-related factors and inflammatory factors were determined by Real-time PCR. Western blot was employed to determine the expression of cAMP pathway-related factors and connexin 43 （Cx43）. ResultsA total of 434 component targets and 545 depression targets were obtained， including 84 common targets， among which 10 core targets were screened out. GO analysis predicted 34 biological processes， 15 cell components， and 11 molecular functions. The KEGG pathways were mainly related to gap junction and cAMP signaling pathway. The core components had good binding affinity with the core targets. The results of animal experiments showed that compared with the control group， CORT prolonged the immobility time of mice in forced swimming and tail suspension tests （P<0.01）， lowered the serum levels of NE， BDNF， and 5-HT （P<0.05）， up-regulated the mRNA levels of nuclear factor-κB （NF-κB） and interleukin-6 （IL-6） in the brain tissue （P<0.05）， and down-regulated the mRNA levels of cyclic adenosine monophosphate effector binding protein （CREB） and BDNF （P<0.05） and the protein levels of protein kinase （PRKACA）， phosphorylation （p）-CREB/CREB， BDNF， and Cx43 （P<0.05） in the brain tissue. Compared with the model group， high-dose MA reduced the immobility time of mice in forced swimming （P<0.05） and tail suspension （P<0.01） tests， raised the serum levels of NE， BDNF， and 5-HT （P<0.01）， down-regulated the mRNA level of NF-κB （P<0.01）， and up-regulated the mRNA level of BDNF （P<0.01） and protein levels of PRKACA， p-CREB/CREB， BDNF， and Cx43 （P<0.05）. ConclusionMA alleviates the CORT-induced depressive behavior of mice. It may play an antidepressant role by regulating cAMP signaling pathway and gap junction pathway， improving synaptic plasticity and gap junction function， and reducing neuroinflammation.

Angelica dahurica,as a medicinal and edible traditional Chinese medicine,is widely used in clinical practice.It is mainly cultivated in Henan,Hebei,Sichuang and Zhejiang provinces.At present,the study found that the main chemical components of this plant contained coumarins,volatile oil,polysaccharides,alkaloids,and amino acids and other components.It has anti-inflammatory,analgesic,anti-oxidant,anti-tumor,whitening effect and other pharmacological activities.In this paper,the chemical composition,pharmacological action of Angelica dahurica were summarized.Based on the core concepts of quality markers,the quality markers of Angelica dahurica were predicted and analyzed from the aspects of plant relativity and chemical component specificity,traditional medicinal properties,traditional efficacy,measurability of chemical components,Sulfur Fumigated,so as to provide reference for establishment and development of quality evaluation system of Angelica dahurica.

A 3-week practice-oriented training course on chronic obstructive pulmonary disease (COPD) management was conducted in December 2020, 34 primary care physicians from township or community health service centers attended the course. The impact of the training course on the knowledge levels of COPD management was evaluated with a questionnaire survey, the questionnaire contained the knowledge of COPD and its management. The survey showed that before the training, the participants had low knowledge levels on the definition of COPD and its risk factors; 67.6% (23/34) were not aware of COPD-related guidelines and new developments, and 17.6%(6/34) had conducted COPD follow-up assessments, pulmonary rehabilitation, and health education; only 8.8% (3/34) had used the improved British Medical Research Council Dyspnea Index (mMRC) and the chronic obstructive pulmonary disease assessment test (CAT) for patient self-assessment; there was no pulmonary function instrument in their units, and only 3 doctors (8.8%) had previously participated in pulmonary function training and knew indications and contraindications of the pulmonary function test, and complete report interpretation; all participants were unable to use common inhalation devices and master inhalation techniques completely and correctly; 11.8% (4/34) had assessed patients′ handling inhalation devices and performing inhalation. After the training, the knowledge levels of COPD clinical features, lung function and inhalation technique were significantly improved, and the scores were significantly increased compared with those before the training ( P<0.001). The study shows that primary care physicians have insufficient knowledge and management skill of COPD. The practice-oriented training can significantly improve the knowledge and skills of primary care physician for COPD management in the community.

Objective To effectively use the clinical data generated in daily operation and to realize information networking based on the existing resources of radiotherapy department. To improve quality management efficiency in radiotherapy process. Methods The radiotherapy process and required documents were analyzed. The reporting tool Microsoft Report Builder, which is based on SQL database, was applied to design the patient documents by extracting and analyzing a large number of data generated by Aria, the existing network of our radiotherapy department. PDCA Tools was used to analyze the weak links in the process. Reports with quantitative indices have been designed according to corresponding countermeasures, so as to improve quality control level of the process. Results More than one thousand patients were treated in our department since 2020. All patient documents of radiotherapy can be archived and inquired online after registration only once. 13 daily statistical reports, 5 quarters and 3 annual reports were scheduled according to practical demands. The waiting time before radiotherapy was shortened from 16.2 days to 14.8 days after operating the reporting system 3 months later. The staff could master the treatment progress of patients easily and patients who interrupted the treatment were found in time. Conclusion The reporting tools can realize patient information extraction and networked management effectively in radiotherapy process. Staff efficiency of personnel work and communication was improved. The resource allocation was optimized according to the report data in real time, improving the efficiency and quality of radiotherapy. This method is generally applicable and practical to radiotherapy department.

Objective:To establish a disease risk prediction model for the newborn screening system of inherited metabolic diseases by artificial intelligence technology.Methods:This was a retrospectively study. Newborn screening data ( n=5 907 547) from February 2010 to May 2019 from 31 hospitals in China and verified data ( n=3 028) from 34 hospitals of the same period were collected to establish the artificial intelligence model for the prediction of inherited metabolic diseases in neonates. The validity of the artificial intelligence disease risk prediction model was verified by 360 814 newborns ' screening data from January 2018 to September 2018 through a single-blind experiment. The effectiveness of the artificial intelligence disease risk prediction model was verified by comparing the detection rate of clinically confirmed cases, the positive rate of initial screening and the positive predictive value between the clinicians and the artificial intelligence prediction model of inherited metabolic diseases. Results:A total of 3 665 697 newborns ' screening data were collected including 3 019 cases ' positive data to establish the 16 artificial intelligence models for 32 inherited metabolic diseases. The single-blind experiment ( n=360 814) showed that 45 clinically diagnosed infants were detected by both artificial intelligence model and clinicians. A total of 2 684 cases were positive in tandem mass spectrometry screening and 1 694 cases were with high risk in artificial intelligence prediction model of inherited metabolic diseases, with the positive rates of tandem 0.74% (2 684/360 814)and 0.46% (1 694/360 814), respectively. Compared to clinicians, the positive rate of newborns was reduced by 36.89% (990/2 684) after the application of the artificial intelligence model, and the positive predictive values of clinicians and artificial intelligence prediction model of inherited metabolic diseases were 1.68% (45/2 684) and 2.66% (45/1 694) respectively. Conclusion:An accurate, fast, and the lower false positive rate auxiliary diagnosis system for neonatal inherited metabolic diseases by artificial intelligence technology has been established, which may have an important clinical value.

Objective: To assess the efficiency and safety of low-dose decitabine in patients with lower-risk myelodysplastic syndrome (MDS) to couple with the clinical significance of MDS-related gene mutations. Methods: This study was done in 4 institutions in Zhejiang Province. A total of 62 newly diagnosed patients with lower-risk MDS were assigned to two groups of decitabine (12 mg·m^-2·d^-1 for 5 consecutive days) and best supportive care (BSC) . Their bone marrow samples were subject to examinations of MDS-related 15 gene mutations. The primary endpoints were the proportion of patients who achieved overall response (ORR) after at least two cycles and progression-free survival (PFS) , and their relevances to the gene mutations. Results: Of 62 enrolled patients, and 51 cases were included in the final analysis. 16 of 24 patients (66.7%) in decitabine group achieved ORR versus 8 of 27 (29.6%) in BSC group (χ²=6.996, P=0.008) ; PFS prolongation of decitabine versus BSC was statistically significant (not reached vs 13.7 months, P=0.037) . Among 51 patients, at least one gene mutation was identified in 20 patients (39.2%) , including 4 single SF3B1 mutation. PFS in cases with gene mutations (not including single SF3B1 mutation) was significantly shorter than of no gene mutation (9.2 months vs 18.5 months, P=0.008) , but not for ORR (37.5% vs 58.1%, P=0.181) . Among 16 patients with mutated genes, ORR in decitabine and BSC groups were 75% (6/8) and 0 (0/8) , respectively. The most adverse events in decitabine group were grade 3 to 4 neutropenia (45.8%) and grade 3 to 4 infections (33.3%) . Conclusion This preliminary study showed that low-dose decitabine produced promising results with an acceptable safety in lower-risk MDS patients, especially for those with mutated genes. Further study targeting poor prognostic lower-risk MDS patients should be warranted.

Objective To evaluate the value of perioperative multimodal stratified analgesia guided by PPRS-CYMZ 2.0. Methods One hundred and sixteen patients of both sexes, aged 16-85 yr, of A-merican Society of Anesthesiologists physical statusⅠ-Ⅲ, scheduled for elective surgery in our hospital in August 2016, were included in this study and assigned into empirical analgesia group(group E, n=79) and stratified analgesia group(group S, n=73). The risk of postoperative pain was estimated by an expe-rienced associate chief anesthesiologist based on his clinical experience, and the perioperative analgesic protocol was determined in group E. The risk of postoperative pain was assessed using the perioperative pain risk scale PPRS-CYMZ 2.0 by another experienced associate chief anesthesiologist, the risk was stratified according to the scores, and the corresponding stratified analgesic protocol was determined in group S. Vis-ual analog scale scores and parents′satisfaction with analgesia were recorded on postoperative day 30. The requirement for preventive analgesia, total pressing times of patient-controlled analgesia(PCA)pump in 0-6 h, 6-24 h and 24-72 h periods, PCA background infusion dose and consumption of rescue analgesics were recorded. The development of adverse events during postoperative hospital stay and postoperative re-covery were also recorded. Analgesia-related parameters of medical economics were calculated. Results There was no significant difference in postoperative pain risk stratification between group E and group S(P>0.05), and the majority of patients were at moderate risk. Compared with group E, no significant change was found in visual analog scale scores on postoperative day 30, PCA background infusion dose or incidence of postoperative adverse effects(P>0.05), the requirement for preventive analgesia and satisfaction scores were significantly increased in high risk patients, the consumption of rescue analgesics was decreased in moderate risk patients(P<0.05), no significant change was found in the total pressing times of PCA pump in each time period in low risk patients(P>0.05), the total pressing times of PCA pump was significantly decreased, and the direct analgesic cost per patient and total analgesic cost were decreased in moderate and high risk patients, and the first ambulation time and length of postoperative hospital stay were shortened in high risk patients in group S(P<0.05). Conclusion PPRS-CYMZ 2.0 can achieve perioperative multi-modal stratified analgesia and individualized treatment.

Castleman disease (CD) is an uncommon non-clonal lymphoproliferative disorder with unknown etiology.No standard therapy is recommended for relapsed/refractory CD patients,thus requiring development of novel experimental approaches.Our cohort of three adult patients with multicentric CD (MCD) were treated with refractory to traditional chemotherapy ienalidomide-containing regimens (10-25 mg lenalidomide perorally administered on days 1-21 in 28-day cycle) as second-to fourth-line treatment.Partial remission was achieved in first plasma-cell CD patient,who relapsed seven months after autologous hematopoietic stem cell transplantation and then failed to respond to four cycles of chemotherapy.Partial remission was obtained in second patient with CD and polyneuropathy,organomegaly,endocrinopathy,monoclonal gammopathy,and skin changes syndrome.Third case showed complete remission with complete disappearance of pleural effusion and ascites and normalization of platelet count.To conclude,encouraging clinical responses were achieved in cohort of three patients with lenalidomide-based regimen,though long-term efficacy remains to be observed.We propose further investigation of therapeutic potential of this drug in treating MCD.