Qiaomai is one of the eight extraordinary meridians,and its theory has long been marginalized in academic research on meridians.So its academic and practical value has not received sufficient attention.This article is based on the theory in Huangdi Neijing,combined with unearthed literature from the Pre-Qin period and the fusion of various medical schools reflected in the meridian theory system,to explore qiaomai's name and essence.Our team believes that the formation of qiaomai is the result of the long-term exploration and application of somatic twisting daoyin in Central Plains medicine.The formation of qiaomai coincides with the practical process and therapeutic thinking of somatic twisting daoyin,which has gone through a transformation from directly treating sick tendons to treating sick qi by adjusting tendons.The name of qiaomai may originate from the meanings of various movements such as limb touching,stretching,and swinging in the somatic twisting technique.The primitive physiological function of qiaomai is to dominate human movement,and its physiological level should be located in the tendons of the human body.Qiaomai constantly intersected and was confused with the bladder meridian of foot-taiyang and the kidney meridian of foot-shaoyin after the integration of meridian theory and visceral medicine during the period of Huangdi Neijing,and the positioning and function of qiaomai gradually became blurred.This cognitive confusion has become the fundamental reason why the academic exploration and clinical application of qiaomai has been hindered for a long time.This also suggests that when studying various Pre-Qin medical theoretical systems in Huangdi Neijing,sufficient screening,analysis,and restoration should be carried out to ensure that theories from different sources are authentic.

Age-related hearing loss(ARHL)is a common chronic disease that poses a serious threat to the physical and mental health of the elderly in an aging society.It is a sensorineural hearing loss characterized by the loss of auditory hair cells,stria vascularis lesions,apoptosis of spiral ganglia,and degeneration of the audi-tory central nervous system,reducing the quality of life of the patients.This article reviews the research progress in the relationship of ARHL with Alzheimer's disease,depression,and frailty,as well as the daily intervention in ARHL.This review aims to improve people's awareness and attention to the health hazards of ARHL and to delay the occurrence and development of ARHL by implementing daily intervention measures to form a healthy lifestyle.

IgA nephropathy (IgAN) is one common type of glomerulonephritis caused by a deposition of immune complexes in mesangium and partial capillary loops. It is also an important risk factor for end-stage renal disease (ESRD). Kidney transplantation (KT) has been an ultimate treatment for IgAN patients progressing into ESRD. However, there is still a high risk of recurrence after transplantation. Currently no effective treatment is available for recurrent IgAN. This review summarized the latest researches of managing IgAN recurrence after KT, such as optimal treatment, immunosuppression, complement therapy and surgery.

Renal interstitial fibrosis (RIF) is the crucial pathway in chronic kidney disease (CKD) leading to the end-stage renal failure. However, the underlying mechanism of Shen Qi Wan (SQW) on RIF is not fully understood. In the current study, we investigated the role of Aquaporin 1 (AQP1) in SQW on tubular epithelial-to-mesenchymal transition (EMT). A RIF mouse model induced by adenine and a TGF-β1-stimulated HK-2 cell model were etablished to explore the involvement of AQP 1 in the protective effect of SQW on EMT in vitro and in vivo. Subsequently, the molecular mechanism of SQW on EMT was explored in HK-2 cells with AQP1 knockdown. The results indicated that SQW alleviated kidney injury and renal collagen deposition in the kidneys of mice induced by adenine, increased the protein expression of E-cadherin and AQP1 expression, and decreased the expression of vimentin and α-smooth muscle actin (α-SMA). Similarly, treatmement with SQW-containing serum significantly halted EMT process in TGF-β1 stimulated HK-2 cells. The expression of snail and slug was significantly upregulated in HK-2 cells after knockdown of AQP1. AQP1 knockdown also increased the mRNA expression of vimentin and α-SMA, and decreased the expression of E-cadherin. The protein expression of vimentin increased, while the expression of E-cadherin and CK-18 significantly decreased after AQP1 knockdown in HK-2 cells. These results revealed that AQP1 knockdown promoted EMT. Furthermore, AQP1 knockdown abolished the protective effect of SQW-containing serum on EMT in HK-2 cells. In sum, SQW attentuates EMT process in RIF through upregulation of the expression of AQP1.
Drugs, Chinese Herbal/pharmacology* ; Humans ; Animals ; Mice ; Male ; Cell Line ; Rats ; Kidney/physiology* ; Fibrosis/drug therapy* ; Renal Insufficiency, Chronic/drug therapy* ; Adenine ; Epithelial-Mesenchymal Transition ; Aquaporin 1/metabolism*

Objective:To study the effect of trefoil factor family (TFF) 3 on the expression of tight junctions (TJs) in the nasal mucosa epithelium of eosinophilic chronic rhinosinusitis (eCRS) and its mechanism.Methods:From September to December 2020, eligible patients from the Department of Otorhinolaryngology of the First Affiliated Hospital of Nanchang University were recruited, including 11 control patients and 37 patients with chronic rhinosinusitis with nasal polyps (CRSwNP), from whom nasal mucosa and nasal polyp tissue samples were collected. Immunohistochemistry (IHC) was used to detect the localization and expression intensity of TFFs (TFF1, TFF2 and TFF3) and TJs (occudin, claudin-1 and ZO-1) in nasal mucosa. Real-time fluorescence quantitative polymerase chain reaction (RT-qPCR) and western blot (WB) were used to detect the mRNA and protein expression. A cell model of tight junction injury in human nasal epithelial cells (HNECs) through stimulation with interleukin (IL)-13 was also established. The optimal modeling concentration and time for HNECs were determined, which were subsequently treated with TFF3 and/or a phosphoinositide 3-kinase (PI3K)-specific inhibitor (LY294002). Finally, RT-qPCR and WB were used to assess the effects of TFF3 on tight junctions and the PI3K/serine/threonine kinase (Akt) signaling pathway. Data were analyzed statistically using GraphPad Prism 7 software.Results:IHC results showed that the expression of TFF1 and TFF3 in nasal mucosa of eCRS group was significantly higher than that of control group ( t=4.62, P=0.002; t=5.89, P<0.001), respectively, mainly expressed in goblet cell. The expression of occludin, claudin-1 and ZO-1 in the nasal mucosa of the eCRS group was lower than that of the control group (occludin t=3.98, P=0.019; claudin-1 t=5.15, P=0.002; ZO-1 t=5.42, P=0.001), respectively. WB results showed that the expression of TFF3 in non-eosinophilic chronic sinusitis (Non-eCRS) group and eCRS group was higher than that in the control group ( t=3.62, P=0.036; t=5.93, P<0.001). The expression of occludin, claudin-1 and ZO-1 in eCRS group was lower than that in the control group (occludin t=5.14, P=0.002; claudin-1 t=6.35, P<0.001; ZO-1 t=6.64, P<0.001), respectively. The RT-qPCR results showed that compared with the control group, the levels of TFF1 and TFF3 mRNA were increased in the nasal mucosal epithelium of the Non-eCRS and eCRS groups (TFF1 t=3.98, P=0.046, t=4.89, P=0.002; TFF3 t=3.50, P=0.044, t=6.78, P<0.001). There was no statistically significant difference in TFF2 mRNA levels between the Non-eCRS and eCRS groups ( t=1.34, P=0.061; t=3.37, P=0.055). Compared with the control group, Non-eCRS and eCRS groups showed a decrease in the mRNA levels of occludin, claudin-1 and ZO-1 (occludin t=4.27, P=0.011, t=5.61, P=0.007; claudin-1 t=3.62, P=0.036, t=6.80, P<0.001; ZO-1 t=3.47, P=0.047, t=7.86, P<0.001). The mRNA levels of TFF3 and TJs in eCRS nasal mucosa tissue showed a moderate positive correlation (occludin r=0.661, claudin-1 r=0.614, ZO-1 r=0.548, all P<0.001); TFF1 showed a low degree of positive correlation with the expression of occludin, claudin-1 and ZO-1 (occludin r=0.467, P=0.040; claudin-1 r=0.362, P=0.012; ZO-1 r=0.425, P=0.025). The establishment of cell models showed that compared with normal HNECs, the mRNA expression of TFF3 was most significantly increased at a concentration of 50 ng/ml stimulated by IL-13 ( t=3.72, P=0.013); The mRNA expression of occludin, claudin-1 and ZO-1 decreased (occludin t=3.18, P=0.031; claudin-1 t=3.86, P=0.010; ZO-1 t=5.16, P=0.002). The expression of TFF3 mRNA increased most significantly after 15 hours of IL-13 stimulation ( t=3.14, P=0.034); The mRNA expression of occludin, claudin-1 and ZO-1 decreased (occludin t=3.97, P=0.010; claudin-1 t=4.78, P=0.004; ZO-1 t=5.16, P=0.004). TJs damage model could be established by treating HNECs with 50 ng/ml IL-13 for 15 hours. Intervention experiments showed that compared with the IL-13 group, the IL-13+TFF3 group showed an increase in TJs mRNA expression (occludin t=6.10, P=0.009; claudin-1 t=5.90, P=0.013; ZO-1 t=9.44, P=0.007). Compared with the IL-13 group, the expression of TJs protein in the IL-13+TFF3 group increased (occludin t=3.23, P=0.013; claudin-1 t=9.40, P=0.017; ZO-1 t=2.23, P=0.032); The expression of TJs protein decreased in the IL-13+TFF3+LY294002 group (occludin t=4.73, claudin-1 t=8.77, ZO-1 t=3.51, all P<0.001). Compared with the IL-13+TFF3 group, the IL-3+TFF3+LY294002 group showed a decrease in PI3K and p-Akt/Akt protein expression (PI3K t=13.29, p-Akt/Akt t=10.30, all P<0.001). The increased mRNA and protein expression of occludin, claudin-1 and ZO-1 induced by TFF3 were also inhibited by LY294002. Conclusion:TFF3 can up-regulate the expression of occludin, claudin-1, and ZO-1 through PI3K/Akt pathway, and has a certain protective effect on the nasal mucosal epithelial barrier, providing a new idea for treating eCRS.

Objective: To investigate the predictive value of the joint prediction model based on the modified systemic inflammatory response syndrome (SIRS) score (hereinafter referred to as the joint prediction model) for the mortality risk of patients with large area burns within 24 hours after admission. Methods: The clinical data of 158 patients [111 males, 47 females, aged 40 (28, 50) years] admitted to the Department of Burn Surgery of the First Affiliated Hospital of Naval Medical University from January 2005 to January 2018, conforming to the study criteria, were analyzed retrospectively by the method of case-control study. The age, gender, total burn area, full-thickness burn area, injury cause, with or without inhalation injury, severity of inhalation injury, and tracheotomy condition of patients were recorded, and the modified SIRS score and the modified Baux score of patients were calculated. According to the final outcome, all patients were divided into survival group (n=123) and death group (n=35). The clinical data of patients between two groups, except for modified Baux score, were compared by chi-square test or Mann-Whitney U test to screen the death-related factors of patients. The indexes with statistically significant difference between the two groups were included in the multivariate logistic regression analysis to screen the independent risk factors related to the death of patients, and the prediction model was constructed by combining the modified SIRS score. The receiver′s operating characteristic curves of the modified SIRS score, the modified Baux score, and the joint prediction model of 158 patients were drawn to analyze their ability to predict death of patients. The area under curve (AUC) of the receiver′s operating characteristic and the sensitivity and specificity of optimal threshold were calculated, and the quality of AUC of the three prediction indexes was compared with Jonckheere-Terpstra test. Results: (1) There were statistically significant differences between the two groups in the modified SIRS score, age, total burn area, full-thickness burn area, severity of inhalation injury, with or without inhalation injury, and tracheotomy condition of patients (Z=-4.356, -3.568, -5.291, -6.052, -4.720, χ²=12.967, 19.692, P<0.01). (2) The modified SIRS score, age, full-thickness burn area were the independent risk factors for the death of patients with large area burn (odds ratio=2.699, 1.069, 1.029, 95% confidence interval=1.447-5.033, 1.029-1.109, 1.005-1.054, P<0.05). (3) The AUC of modified SIRS score, the joint prediction model, and the modified Baux score for predicting death of 158 patients within 24 hours after admission were 0.730, 0.879, and 0.895 respectively (95% confidence interval=0.653-0.797, 0.818-0.926, 0.836-0.938, P<0.01). The sensitivities of the three optimal threshold values to death prediction were 54.3%, 91.4%, and 82.9% respectively, while the specificities were 81.3%, 76.4%, and 84.6% respectively. The AUC quality of the joint prediction model was similar to that of the modified Baux score (95% confidence interval=-0.057-0.088, P>0.05), and both of them were significantly better than that of the modified SIRS score (95% confidence interval=0.072-0.259, 0.023-0.276, P<0.05 or P<0.01). Conclusions Both the joint prediction model and the modified Baux score are considered to be good to predict the death rate of patients with large area burns at early stage after admission. However, the joint prediction model has better clinical practice value due to its advantage of simple scoring and easier access to data acquisition.

The expression of histone lysine-specific demethylase 1 (LSD1) in colorectal cancer cells is increased, and LSD1 is closely related to its occurrence, development, proliferation, invasion and metastasis. LSD1 is a demethylase whose function depends on flavin adenine dinucleoside. It can specifically catalyze the demethylation reaction of histone lysine, and regulate the expression of target genes by reaction of demethyl and dimethyl (H3K4me, H3K4me2, H3K9me, and H3K9me2) at the 4th and 9th positions of lysine H3. Targeted inhibition of LSD1 has been proved to be able to exert significant anti-tumor effect, but since the tumors involve multiple centers and factors, later studies have found that single inhibition of LSD1 cannot completely and effectively kill tumor cells. Moreover, the specificity of the LSD1 catalytic substrate depends to a large extent on the synergistic factors that bind to it and form complexes. The double-target inhibitors based on LSD1 shows more remarkable effect in tumor inhibition. Therefore, finding the combined synergistic factors of LSD1 may provide the basis for the research of multi-target inhibitors.

Objective:To Chinesize Post-Event Processing Inventory Trait (PEPI-T) and verify the reliability and validity of its application in high school students.Methods:First, the PEPI-T was translated and pre-measured, then the wording according to the pre-measurement results was adjusted and back-translated.Then, the Chinese version of PEPI-T(PEPI-T-C) was finalized.In total, 947 adolescents aged from 15 to 19 were recruited to complete Social Anxiety Scale for Adolescents, Short Mood and Feelings Questionnaire, General Self-Efficacy Scale and PEPI-T-C, which were used as validity indicator.Results:Confirmatory factor analysis results showed that the PEPI-T-C still followed the three dimentions of self-judgement, frequency and intensity of the original scale and showed good model fit indices (χ 2/ df=2.59, RMSEA=0.04, CFI=0.97, TLI=0.95, SRMR=0.03). The internal consistency coefficients for PEPI-T-C was 0.78, while the three subscales was (0.44-0.75). PEPI-T-C and its subscales were significantly correlated with social anxiety and depression ( r=0.22-0.43, all P<0.01). The subscale of intensity showed significant correlation with self-efficacy( r=-0.11, P<0.01). PEPI-T-C and its subscale of self-judgement and frequency showed no significant correlations with self-efficacy( P>0.05). Conclusions:PEPI-T-C showed an acceptable reliabilities and validities in Chinese high school students, and would be used to assess their post-event rumination.Future research should examine the psychometric properties of PEPI-T-C in other Chinese adolescents’ samples.

Objective To study the influences on the production of major inflammatory cytokines after co-culturing macrophages with human umbilical vein endothelial cells ( HUVECs) that were infected with dengue virus type 2 (DENV-2). Methods Density gradient centrifugation was used to isolate periph-eral blood mononuclear cells ( PBMC) from concentrated human leukocytes. Adherent monocytes in culture flasks were obtained and stimulated with macrophage colony-stimulating factor ( M-CSF) to prepare macro-phages. The purity of CD14+CD11b+ cells was measured by flow cytometry. Changes in the expression of NS1 at mRNA level in HUVECs were detected by real-time PCR following DENV-2 infection. DENV-2-in-fected HUVECs were co-culture with macrophages in Transwell chambers. A control group was set up by pre-treating HUVECs with sphingosine-1-phosphate (S1P) type 1 (S1P1)-specific receptor agonist CYM-5442 for 24 h to remove the drug before infection and then co-culturing the infected cells with macrophages. Real-time PCR was used to detect the expression at mRNA level of IL-6 and IL-8 in HUVECs and IL-6, IL-8, TNF-α and IL-1β in macrophages. A double-antibody sandwich ELISA was used to detect the expression of above cytokines in culture supernatants. Results After HUVECs were infected with DENV-2, expression of NS1 gene at mRNA level gradually increased to the peak at 24 h (2. 66±0. 53, P<0. 05) and then de-creased. The purity of macrophages detected by flow cytometry was (89. 16±2. 07) ％. Expression of IL-6 and IL-8 at mRNA level in DENV-2-infected HUVECs was up-regulated. The peak values reached at 24 h of IL-6 and IL-8 expression were 16. 10±0. 17 and 29. 76±0. 58, while the expression levels at 24 h in the un-infected group were 1. 46±0. 67 and 1. 60±0. 54, respectively. Expression of IL-6, IL-8, TNF-αand IL-1βat mRNA level in DENV-2-infected macrophages was increased significantly. The levels of IL-6, IL-8, TNF-αand IL-1β expression at 24 h were 45. 82±3. 72, 52. 34±1. 69 (12 h), 8. 94±1. 75 and 30. 96±1. 44 in the infected macrophages, and 1. 16±0. 22, 1. 15±0. 21, 1. 11±0. 09 and 1. 47±0. 31 in the uninfected group. Expression of these cytokines was decreased at every time points after co-culturing of DENV-2-infec-ted HUVECs with macrophages, but still significantly higher than that in the uninfected group. In the co-cul-ture group with DENV-2 infection, CYM-5442 pretreatment significantly decreased the expression at mRNA level of IL-6 and IL-8 in HUVECs (P<0. 01) and that of IL-6, IL-8, TNF-αand IL-1βin macrophages (P<0. 01). Conclusions DENV-2 could infect primary HUVECs, and then activate macrophages to promote the secretion of large amounts of IL-6, IL-8, TNF-αand IL-1β. Moreover, the activated macrophages could reduce the production of inflammatory cytokines in HUVECs to a certain extent.

In this study, the necessity of professional master's degree training in clinical pharmacy was analyzed by means of literature research and practice summary, and the existing problems in current professional curriculum, tutor team and practice teaching were discussed. In view of the existing problems, this paper puts forward that medical colleges and universities should give full play to their medical resources, draw lessons from the talents training experience of clinical pharmacists training base, adopt measures such as optimizing curriculum system, selecting tutors, attaching importance to practical teaching, so as to improve the quality of postgraduate training in clinical pharmacy, train high-level clinical pharmacists, and promote the development of clinical pharmacy in China.