Based on the duality of "healthy" and "pathogenic" of the immune system in physiological and pathological states， and combined with the analogy between "immune function" and "healthy qi"， the theory of "transformation of healthy qi into pathogenic qi" was proposed to guide the pattern identification and treatment of autoimmune diseases. The theory of "transformation of healthy qi into pathogenic qi" means that "healthy qi"， which is originally used by the body's original ability to defend and remove harmful factors or normal functional activities， transformed into "pathogenic qi"， which is factors that damage and destroy the human body or abnormal body state. In the pathogenesis of autoimmune diseases， the pathogenic factors and causes of congenital endowment， tissue damage under the influence of external pathogens， abnormal function of zang-fu （脏腑） organs and meridians， abnormal transmission and transformation of qi， blood， body fluids was proposed. Autoimmune diseases have the dynamic mechanism of latent pathogen at early stage， internal and external contraction at the onset stage， and the expansion of the pathogenic qi at the complete period， and also have the characteristics of the specificity， invisibility and contradiction of healthy qi and pathogenic qi. In terms of treatment， it advocates the ideas of treatment with both attack and supplementation throughout the disease， identifying diseases with special prescriptions and formulas for specific diseases， dynamically adjusting treatment by identifying the remission and onsets of the disease， observing the changes in the dynamics of healthy qi transforming into pathogenic qi， and treating disease before it arises with early intervention.

Objective:To evaluate the efficacy and safety of hypomethylating agents (HMA) in patients with myelodysplastic syndromes (MDS) .Methods:A total of 409 MDS patients from 45 hospitals in Zhejiang province who received at least four consecutive cycles of HMA monotherapy as initial therapy were enrolled to evaluate the efficacy and safety of HMA. Mann-Whitney U or Chi-square tests were used to compare the differences in the clinical data. Logistic regression and Cox regression were used to analyze the factors affecting efficacy and survival. Kaplan-Meier was used for survival analysis. Results:Patients received HMA treatment for a median of 6 cycles (range, 4-25 cycles) . The complete remission (CR) rate was 33.98% and the overall response rate (ORR) was 77.02%. Multivariate analysis revealed that complex karyotype ( P=0.02, OR=0.39, 95% CI 0.18-0.84) was an independent favorable factor for CR rate. TP53 mutation ( P=0.02, OR=0.22, 95% CI 0.06-0.77) was a predictive factor for a higher ORR. The median OS for the HMA-treated patients was 25.67 (95% CI 21.14-30.19) months. HMA response ( P=0.036, HR=0.47, 95% CI 0.23-0.95) was an independent favorable prognostic factor, whereas complex karyotype ( P=0.024, HR=2.14, 95% CI 1.10-4.15) , leukemia transformation ( P<0.001, HR=2.839, 95% CI 1.64-4.92) , and TP53 mutation ( P=0.012, HR=2.19, 95% CI 1.19-4.07) were independent adverse prognostic factors. There was no significant difference in efficacy and survival between the reduced and standard doses of HMA. The CR rate and ORR of MDS patients treated with decitabine and azacitidine were not significantly different. The median OS of patients treated with decitabine was longer compared with that of patients treated with azacitidine (29.53 months vs 20.17 months, P=0.007) . The incidence of bone marrow suppression and pneumonia in the decitabine group was higher compared with that in the azacitidine group. Conclusion:Continuous and regular use of appropriate doses of hypomethylating agents may benefit MDS patients to the greatest extent if it is tolerated.

Objective To analyze the correlation of inflammatory markers C-reactive proten(CRP),serum amyloid protein A(SAA),interleukin-6(IL-6)levels and subjective sleep characteristics in patients with first-episode acute cerebral infarction.Methods A total of 113 patients with first-episode cerebral infarction admitted to the Department of Neurology,the People's Hospital of Fuyang from March 2022 to April 2023 were prospectively and continuously selected as subjects.According to the Pittsburgh sleep quality index(PSQI),they were divided into insomnia group(PSQI＞7 points)and non-insomnia group(PSQI ≤7 points).General demo-graphic data and differences in CRP,SAA,IL-6 levels,Hamilton anxiety scale(HAMA)and Hamilton depression scale(HAMD)scores were compared between the two groups.Partial correlation analysis was used to analyze the correlation between three serum markers and PSQI effect factors.Results There were no significant differences in age,gender,baseline NIHSS score and mRS score between the two groups(P＞0.05).HAMD scores(z=-3.993,P＜0.001),HAMA scores(z=-3.806,P＜0.001),CRP,IL-6,SAA(P＜0.001)in insomnia group were significantly higher than those in non-insomnia group.The history of hyperlipidemia between the two groups was statistically significant(z=5.913,P=0.015).Multivariate Logisitic regression analysis showed that CRP(OR=1.55,P＜0.01),HAMD scores,HAMA scores and hyperlipidemia were independent risk factors for chronic insomnia in patients with first-episode cerebral infarction,and HAMD scores had a greater effect than HAMA scores(OR:1.10 vs 1.04).Partial correlation analysis showed that IL-6 and CRP levels were significantly correlated with the total score of PSQI(P＜0.05),while SAA was not significantly correla-ted with the total score of PSQI(P＞0.05).IL-6 level was positively correlated with sleep quality(r=0.231)sleep efficiency(r=0.322)and sleep duration(r=0.221).SAA level was positively correlated with sleep efficiency(r=0.242),while CRP level was posi-tively correlated with sleep latency(r=0.194),sleep duration(r=0.247)and sleep efficiency(r=0.225).Conclusion The inflam-matory markers CRP,IL-6 and SAA levels were elevated in the patients with first-episode cerebral infarction accompanied by insomnia,which were correlated with the severity of insomnia.The correlation between CRP and IL-6 levels and sleep characteristics was consistent with each other.

Non-coding RNAs (ncRNAs) are a class of functional RNAs that play critical roles in different diseases. NcRNAs include microRNAs, long ncRNAs, and circular RNAs. They are highly expressed in the brain and are involved in the regulation of physiological and pathophysiological processes of central nervous system (CNS) diseases. Mounting evidence indicates that ncRNAs play key roles in CNS diseases. Further elucidating the mechanisms of ncRNA underlying the process of regulating glial function that may lead to the identification of novel therapeutic targets for CNS diseases.
Humans ; RNA, Untranslated/genetics* ; MicroRNAs/genetics* ; RNA, Long Noncoding/genetics* ; RNA, Circular ; Central Nervous System Diseases/genetics*

Objective: This study’s objective is to assess the efficacy and safety of Pulsed Magnetic Therapy System (PMTS) in improving insomnia disorder. Methods: Participants with insomnia disorder were randomly assigned to receive either PMTS or sham treatment for four weeks (n= 153; PMTS: 76, sham: 77). Primary outcomes are the Insomnia Severity Index (ISI) scores at week 0 (baseline), 1, 2, 3, 4 (treatment), and 5 (follow-up). Secondary outcomes are the Pittsburgh Sleep Quality Index at baseline and week 4, and weekly sleep diary-derived values for sleep latency, sleep efficiency, real sleep time, waking after sleep onset, and sleep duration. Results: The ISI scores of the PMTS group and the sham group were 7.13±0.50, 11.07±0.51 at week 4, respectively. There was a significant group×time interaction for ISI (F3.214, 485.271=24.25, p<0.001, ηp 2=0.138). Only the PMTS group experienced continuous improvement throughout the study; in contrast, the sham group only experienced a modest improvement after the first week of therapy. At the end of the treatment and one week after it, the response of the PMTS group were 69.7% (95% confidence interval [CI]: 58.6%–79.0%), 75.0% (95% CI: 64.1%–83.4%), respectively, which were higher than the response of the sham group (p<0.001). For each of the secondary outcomes, similar group×time interactions were discovered. The effects of the treatment persisted for at least a week. Conclusion PMTS is safe and effective in improving insomnia disorders.

Objective:To summary the mixed infection as well as clinical characteristics and analyze the risk factors for mixed infection of severe adenovirus pneumonia(SAP) in children.Methods:The clinical data of 114 children with SAP were retrospectively analyzed.Multivariate Logistic regression analysis was performed to assess the risk factors for mixed infection.Results:The incidence age was from 6 months to 2 years(62.5%). High fever(94.7%), cough(98.2%), dyspnea(86.8%) and lethargy(95.6%) were the main symptoms.Laboratory examination showed that children with SAP were prone to increased white blood cell count, C-reactive protein, procalcitonin, aspartate aminotransferase, alanine aminotransferase and CK-MB, as well as decreased proportion of CD3 + , CD4 + , CD8 + , CD4 + /CD8 + and NK cells.The main complications intrapulmonary organ were respiratory failure(80.7%). The main complications extrapulmonary organ were circulatory complications (55.3%). SAP was easily combined with other pathogenic infections.Streptococcus pneumoniae(22.9%)was the most common bacterial pathogen.Respiratory syncytial virus(10.0%)were the most common virus, in addition, mycoplasma pneumoniae(17.1%) was also common.Multivariable Logistic regression analysis showed that the decreasing ratio of CD4 + /CD8 + and NK cells, congenital heart disease and congenital airway dysplasia were the independent risk factors for mixed infection of SAP in children( P<0.05). Conclusion:The SAP patients could easily suffer from mixed infection and high fatality rate.Immune dysregulation is the important risk factors for mixed infection of SAP in children.So immunoregulatory treatment is very important.

Objective: To investigate the effect of long-chain non-coding RNA Fez family zinc finger protein 1 antisense RNA1 (lncRNA FEZF1-AS1) on the biological function of hepatocellular carcinoma (HCC). Methods: SMMC771 and BEL-7402 cells were transfected with sh-FEZF1-AS1 and OE-FEZF1-AS1, respectively. The expression of lncRNA FEZF1-AS1 was detected by real-time quantitative PCR. Cell proliferation was detected by Cell Counting Kit-8 (CCK-8), and apoptosis was detected by flow cytometry. The effects of lncRNA FEZF1-AS1 on invasion and migration were detected by Transwell and wound healing assays. The expression levels of adhesion molecules were detected by Western blot. The effect of lncRNA FEZF1-AS1 on the in vivo growth was verified by nude mice xenograft experiments. Results: The silencing or ectopic expression of lncRNA FEZF1-AS1 inhibited or promoted the proliferation of hepatocellular carcinoma cells. CCK-8 assay showed that the proliferation abilities of SMMC7721 and BEL-7402 cells in sh-FEZF1-AS1 transfection group significantly decreased, achieving (35.43±4.06)% and (34.68±3.97)%, respectively, on the fifth day. There were significant differences between sh-FEZF1-AS1 group and sh-NC group [52.21±8.46)% and (53.76±7.64)%] (all P<0.05). In contrast, the proliferation ability of SMMC7721 and BEL-7402 cells transfected with OE-FEZF1-AS1 was significantly increased, achieving (83.49±6.92)% and (80.31±3.13)%, respectively, on the fifth day. There were significant differences between OE-FEZF1-AS1 and OE-NC group [53.03±8.84)% and (55.11±7.09)%] (all P<0.05). The subsequent flow cytometry results showed that cell apoptotic rates of SMMC7721 and BEL-7402 cells transfected with sh-FEZF1-AS1 were (13.02±1.38)% and (11.88±1.29)%, respectively, which were significantly higher than those in sh-NC groups [(5.57±1.46)% and (8.06±1.42)%, respectively, all P<0.05]. In contrast, the apoptotic rates of SMMC7721 and BEL-7402 cells transfected with OE-FEZF1-AS1 were (3.01±0.39)% and (3.22±0.43)%, which were significantly lower than those in OE-NC groups [(6.68±0.96)% and (6.63±0.45)%, all P<0.05]. In addition, knockdown or overexpression of lncRNA FEZF1-AS1 expression inhibited or enhanced the migration and invasion abilities as well as the levels of adhesion molecules in hepatocellular carcinoma cells. After 30 days of feeding under the same conditions, the tumor volumes of sh-FEZF1-AS1 and sh-NC SMMC7721 cells xenograft mice models were (0.26±0.03) cm³ and (0.63±0.06) cm³, respectively, showing significant difference (P<0.05). The tumor volumes of sh-FEZF1-AS1 and sh-NC BEL-7402 cells were (0.31±0.02) cm³ and (0.72±0.08) cm³, and the difference was statistically significant (P<0.05). Conclusion lncRNA FEZF1-AS1 may strengthen the growth, migration and invasion of hepatocellular carcinoma cells.

Objective To investigate the effect of long?chain non?coding RNA Fez family zinc finger protein 1 antisense RNA1 ( lncRNA FEZF1?AS1) on the biological function of hepatocellular carcinoma (HCC). Methods SMMC771 and BEL?7402 cells were transfected with sh?FEZF1?AS1 and OE?FEZF1?AS1, respectively. The expression of lncRNA FEZF1?AS1 was detected by real?time quantitative PCR. Cell proliferation was detected by Cell Counting Kit?8 ( CCK?8), and apoptosis was detected by flow cytometry. The effects of lncRNA FEZF1?AS1 on invasion and migration were detected by Transwell and wound healing assays. The expression levels of adhesion molecules were detected by Western blot. The effect of lncRNA FEZF1?AS1 on the in vivo growth was verified by nude mice xenograft experiments. Results The silencing or ectopic expression of lncRNA FEZF1?AS1 inhibited or promoted the proliferation of hepatocellular carcinoma cells. CCK?8 assay showed that the proliferation abilities of SMMC7721 and BEL?7402 cells in sh?FEZF1?AS1 transfection group significantly decreased, achieving (35.43± 4.06)% and ( 34.68± 3.97)%, respectively, on the fifth day. There were significant differences between sh?FEZF1?AS1 group and sh?NC group [52.21 ± 8.46)% and (53.76 ± 7.64)%] ( all P＜0.05). In contrast, the proliferation ability of SMMC7721 and BEL?7402 cells transfected with OE?FEZF1?AS1 was significantly increased, achieving (83.49±6.92)% and (80.31 ± 3.13)%, respectively, on the fifth day. There were significant differences between OE?FEZF1?AS1 and OE?NC group [53.03 ± 8.84)% and ( 55.11 ± 7.09)%] ( all P＜0.05). The subsequent flow cytometry results showed that cell apoptotic rates of SMMC7721 and BEL?7402 cells transfected with sh?FEZF1?AS1 were ( 13.02 ± 1.38)% and ( 11.88 ± 1.29)%, respectively, which were significantly higher than those in sh?NC groups [(5.57±1.46)% and (8.06±1.42)%, respectively, all P＜0.05]. In contrast, the apoptotic rates of SMMC7721 and BEL?7402 cells transfected with OE?FEZF1?AS1 were (3.01 ± 0.39)% and ( 3.22 ± 0.43)%, which were significantly lower than those in OE?NC groups [(6.68±0.96)% and (6.63±0.45)%, all P＜0.05]. In addition, knockdown or overexpression of lncRNA FEZF1?AS1 expression inhibited or enhanced the migration and invasion abilities as well as the levels of adhesion molecules in hepatocellular carcinoma cells.After 30 days of feeding under the same conditions, the tumor volumes of sh?FEZF1?AS1 and sh?NC SMMC7721 cells xenograft mice models were (0.26±0.03) cm3 and (0.63±0.06) cm3, respectively, showing significant difference (P＜0.05). The tumor volumes of sh?FEZF1?AS1 and sh?NC BEL?7402 cells were (0.31±0.02) cm3 and (0.72±0.08) cm3, and the difference was statistically significant ( P＜0.05). Conclusion lncRNA FEZF1?AS1 may strengthen the growth, migration and invasion of hepatocellular carcinoma cells.

Objective To investigate the effect of long?chain non?coding RNA Fez family zinc finger protein 1 antisense RNA1 ( lncRNA FEZF1?AS1) on the biological function of hepatocellular carcinoma (HCC). Methods SMMC771 and BEL?7402 cells were transfected with sh?FEZF1?AS1 and OE?FEZF1?AS1, respectively. The expression of lncRNA FEZF1?AS1 was detected by real?time quantitative PCR. Cell proliferation was detected by Cell Counting Kit?8 ( CCK?8), and apoptosis was detected by flow cytometry. The effects of lncRNA FEZF1?AS1 on invasion and migration were detected by Transwell and wound healing assays. The expression levels of adhesion molecules were detected by Western blot. The effect of lncRNA FEZF1?AS1 on the in vivo growth was verified by nude mice xenograft experiments. Results The silencing or ectopic expression of lncRNA FEZF1?AS1 inhibited or promoted the proliferation of hepatocellular carcinoma cells. CCK?8 assay showed that the proliferation abilities of SMMC7721 and BEL?7402 cells in sh?FEZF1?AS1 transfection group significantly decreased, achieving (35.43± 4.06)% and ( 34.68± 3.97)%, respectively, on the fifth day. There were significant differences between sh?FEZF1?AS1 group and sh?NC group [52.21 ± 8.46)% and (53.76 ± 7.64)%] ( all P＜0.05). In contrast, the proliferation ability of SMMC7721 and BEL?7402 cells transfected with OE?FEZF1?AS1 was significantly increased, achieving (83.49±6.92)% and (80.31 ± 3.13)%, respectively, on the fifth day. There were significant differences between OE?FEZF1?AS1 and OE?NC group [53.03 ± 8.84)% and ( 55.11 ± 7.09)%] ( all P＜0.05). The subsequent flow cytometry results showed that cell apoptotic rates of SMMC7721 and BEL?7402 cells transfected with sh?FEZF1?AS1 were ( 13.02 ± 1.38)% and ( 11.88 ± 1.29)%, respectively, which were significantly higher than those in sh?NC groups [(5.57±1.46)% and (8.06±1.42)%, respectively, all P＜0.05]. In contrast, the apoptotic rates of SMMC7721 and BEL?7402 cells transfected with OE?FEZF1?AS1 were (3.01 ± 0.39)% and ( 3.22 ± 0.43)%, which were significantly lower than those in OE?NC groups [(6.68±0.96)% and (6.63±0.45)%, all P＜0.05]. In addition, knockdown or overexpression of lncRNA FEZF1?AS1 expression inhibited or enhanced the migration and invasion abilities as well as the levels of adhesion molecules in hepatocellular carcinoma cells.After 30 days of feeding under the same conditions, the tumor volumes of sh?FEZF1?AS1 and sh?NC SMMC7721 cells xenograft mice models were (0.26±0.03) cm3 and (0.63±0.06) cm3, respectively, showing significant difference (P＜0.05). The tumor volumes of sh?FEZF1?AS1 and sh?NC BEL?7402 cells were (0.31±0.02) cm3 and (0.72±0.08) cm3, and the difference was statistically significant ( P＜0.05). Conclusion lncRNA FEZF1?AS1 may strengthen the growth, migration and invasion of hepatocellular carcinoma cells.

Cervical cancer is one of the leading causes of death in women with malignancies worldwide.Brachytherapy plays an essential role in the radiation therapy for cervical cancer, and its combination with external beam radiation is indicated for previously untreated or recurrent cervical cancer at various stages without distant metastasis.Magnetic resonance imaging (MRI) has superior resolution of soft tissue, which allows for accurate delineation of target volume, protects organs at risk (OARs), and thus improves treatment outcomes.In recent years, many studies have demonstrated the feasibility and superiority of three-dimensional MRI-guided brachytherapy for cervical cancer.This article aims to elaborate on relevant MRI techniques, selection of applicators, delineation of target volume and OARs, evaluation of treatment plans, and the clinical effect of three-dimensional MRI-guided brachytherapy.