After the definition and emergence of MOOC and its development at home and abroad were described, the position of library under MOOC environment was discussed with stress laid on how to deepen the service in medical library by making use of MOOC and the challenges medical library is faced.

AIM: To explore the effect of atorvastatin on the expression of α-SMA and TGF-β1 in the adventi-tia of ApoE-/-mice with atherosclerosis, and to investigate the underlying mechanism of atorvastatin therapy.METHODS:Male ApoE-/-mice (n =40) at 6-weeks of age were used to establish the atherosclerosis model by feeding with high fat diet. The mice were randomly divided into model group and atorvastatin group.In atorvastatin group, the mice were lavaged with atorvastatin at dose of 20 mg? kg-1? d-1 .The mice in model group were given normal saline.C57BL/6 mice of the same age served as control group, feeding with ordinary food.The mice were respectively sacrificed at the time points of 10 and 15 weeks after feeding with different diets.The ascending aorta was removed for serial sectioning.Some sections were per-formed with Movat staining in order to observe the morphological changes of the tissues, and to measure the relative athero-sclerotic plaque area and the thickness of the adventitia.Some sections were stained with Sirius red to identify the collagen synthesis.Immunohistochemistry assay was prepared to observe the expression of α-SMA and TGF-β1 in the adventitia at different time points.The expression of TGF-β1 at mRNA and protein levels in the thoracoabdominal aorta was measured by RT-qPCR and Western blot.RESULTS: Compared with model group, the formation of plaque in atorvastatin group signifi-cantly descended.Meanwhile the adventitial thickness and collagen synthesis also decreased.The results of immunohisto-
chemical staining showed that compared with 10 weeks-model group, α-SMA and TGF-β1 in 15 weeks-model group was in-creased.The expression of α-SMA and TGF-β1 in atorvastatin group decreased significantly compared with model group. The expression of TGF-β1 at mRNA and protein levels in model group were higher than those in control group.They de-creased in atorvastatin group compared with model group.Compared with 10 weeks-model group, the mRNA and protein of TGF-β1 in 15 weeks-model group were increased.CONCLUSION: Atorvastatin modulates adventitial fibroblast phenotype differentiation by suppressing expression of TGF-β1 and intervenes atherosclerotic development in ApoE.

Background: and Purpose: Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is the most-common form of autoimmune encephalitis, but its early diagnosis is challenging.This study aimed to identify the risk factors for a poor prognosis in anti-NMDAR encephalitis and construct a prognostic composite score for obtaining earlier predictions of a poor prognosis. Methods: We retrospectively analyzed the clinical data, laboratory indexes, imaging findings, and electroencephalogram (EEG) data of 60 patients with anti-NMDAR encephalitis. The modified Rankin Scale (mRS) scores of patients were collected when they were discharged from the hospital. The mRS scores were used to divide the patients into two groups, with mRS scores of 3–6 defined as a poor prognosis. Logistic regression analysis was used to analyze independent risk factors related to a poor prognosis. Results: This study found that 23 (38.3%) and 37 (61.7%) patients had good and poor prognoses, respectively. Logistic regression analysis showed that age, disturbance of consciousness at admission, and ≥50% slow waves on the EEG were significantly associated with patient outcomes. An age, consciousness, and slow waves (ACS) composite score was constructed to predict the prognosis of patients with anti-NMDAR encephalitis at an early stage based on regression coefficients. Conclusions Age, disturbance of consciousness at admission, and ≥50% slow waves on the EEG were independent risk factors for a poor prognosis. The ACS prognostic composite score could play a role in facilitating early predictions of the prognosis of anti-NMDAR encephalitis.

Objective To explore the effect of nicotinamide transmethylase on intracellular reactive oxygen species(ROS)in iron death of hepatocellular carcinoma cells and its mechanism.Methods Methyl nicotinamide(MNA)expression in cells was detected using a tandem liquid chromatography-mass spectrometry.The average fluorescence intensity of ROS and lipid peroxidation was measured using a flow cytometer.Western blot was used to detect changes in the expression of human liver cancer cells(SK-Hep-1,Hep3B).Forty patients with primary hepatocellular carcinoma who received treatment in our hospital from March 2019 to February 2020 were selected as the study subjects,and their adjacent tissue samples and liver cancer tissue samples were collected.Immunohistochemical methods were used to detect the levels of nicotinamide N-methyltransferase(NNMT)and ROS in adjacent and liver cancer tissues.CCK-8 method was used to detect the survival activity of cells with different iron concentrations.Results The MNA levels in the liver cancer tissue group were higher than those in the adjacent tissue group(P<0.05).Compared with the adjacent tissue group,the average fluorescence intensity expression of ROS in the liver cancer tissue group increased,while the average fluorescence intensity expression of lipid peroxidation decreased(P<0.05).Compared with the adjacent tissue group,the expression levels of SK Hep-1 and Hep3B cells in the liver cancer tissue group increased(P<0.05).Compared with the control group,NNMT groups 2,10,20,and 25 μmol/L The cell survival activity level increased(P<0.05);Compared with the NNMT group,the iron inhibition group had different iron concentrations(2μmol/L,10μmol/L,20μmol/L,25μmol/L.The expression of cell viability decreased(P<0.05).Conclusion ROS mediated by nicotinamide methyltransferase can be guided to produce ROS and energy disorders,leading to increased tumor cell death.

Buyang Huanwu Decoction (BYHWD) is a well-known traditional Chinese medicine prescription which is used to treat ischaemic stroke and stroke-induced disabilities. However, the exact mechanism underlying BYHWD's amelioration of ischaemic stroke and its effective constituents remain unclear. The present study aimed to identify the effective constituents of BYHWD and to further explore its action mechanisms in the amelioration of ischaemic stroke by testing the activities of 15 absorbable chemical constituents of BYHWD with the same methods under the same conditions. The following actions of these 15 compounds were revealed: 1) Ferulic acid, calycosin, formononetin, astrapterocarpan-3-O-β-D-glucoside, paeonol, calycosin-7-O-β-D-glucoside, astraisoflavan-7-O-β-D-glucoside, ligustrazine, and propyl gallate significantly suppressed concanavalin A (Con A)-induced T lymphocyte proliferation; 2) Propyl gallate, calycosin-7-O-β-D-glucoside, paeonol, and ferulic acid markedly inhibited LPS-induced apoptosis in RAW264.7 cells; 3) Propyl gallate and formononetin significantly inhibited LPS-induced NO release; 4) Hydroxysafflor yellow A and inosine protected PC12 cells against the injuries caused by glutamate; and 5) Formononetin, astragaloside IV, astraisoflavan-7-O-β-D-glucoside, inosine, paeoniflorin, ononin, paeonol, propyl gallate, ligustrazine, and ferulic acid significantly suppressed the constriction of the thoracic aorta induced by KCl in rats. In conclusion, the results from the present study suggest that BYHWD exerts its ischaemic stroke ameliorating activities by modulating multiple targets with multiple components.
Animals ; Apoptosis ; drug effects ; Brain Ischemia ; drug therapy ; physiopathology ; Drugs, Chinese Herbal ; administration & dosage ; chemistry ; Glucosides ; administration & dosage ; analysis ; Isoflavones ; administration & dosage ; analysis ; Male ; Mice ; Mice, Inbred BALB C ; Monoterpenes ; administration & dosage ; analysis ; PC12 Cells ; RAW 264.7 Cells ; Rats ; Rats, Sprague-Dawley ; Saponins ; administration & dosage ; analysis ; Stroke ; drug therapy ; physiopathology ; Triterpenes ; administration & dosage ; analysis

Objective:To study the relationship between zoledronic acid (ZOL) and vascular endothelial growth factor (VEGF) conformation so as to reveal the mechanism of bisphosphonates inhibiting angiogenesis.Methods:The binding structures of ZOL and VEGF were preprocessed and the molecular dockings were simulated through AutoDockTools, Discovery studio4 and AutoDockVina. The best binding conformation was accurately screened. The effects of various concentrations of ZOL (group A was 0 μmol/L, groups B, C and D were 25, 50 and 100 μmol/L, respectively) on human umbilical vein endothelial cell (HUVEC) proliferation, angiogenesis and angiogenic molecules were detected by using cell counting kit-8 (CCK-8) in vivo and in vitro angiogenesis, immunofluorescence and Western blotting. Results:There was a ZOL binding site on the target protein VEGF conformation. The affinity was -5.2 kcal/mol. This binding site consisted of the hydrophobic region composed of amino acids Cys26, 51, 57, etc. and the hydrogen bond binding region of the A chain (ASP34, SER50) and B chain (CYS61, 68, LEU66, GLY59). The results of CCK-8 showed that the levels of value A in groups B, C and D were significantly lower than that in group A at each time point from 3 to 6 days ( P<0.05). In vitro vascular experiments demonstrated that the numbers of budding in groups B, C and D [(208±28), (151±21) and (62±9), respectively] were significantly lower than that in group A (276±30) ( P<0.05). In vivo vascular experiments displayed that the ratio of Matrigel gel/plasma fluorescence in group A (0.003 1±0.000 3) was significantly higher than those in group B (0.002 1±0.000 2), group C (0.001 6±0.000 2) and group D (0.000 6±0.000 1) ( P<0.05). The results of Western blotting revealed that the expression of VEGF in groups B, C and D [(0.72±0.11), (0.41±0.07) and (0.24±0.04), respectively] were significantly lower than that in group A (1.01±0.02) ( P<0.05), and the expression levels of hypoxia-inducible factor-1α (HIF-1α) in groups B, C and D [(0.68±0.09), (0.55±0.06) and (0.43±0.08), respectively] were significantly lower than that in group A (0.96±0.04) ( P<0.05). Conclusions:ZOL could inhibit cell proliferation, in vivo and in vitro vascularization and expression of VEGF/HIF-1α. The binding site of ZOL with the conformation of VEGF was located in the hydrophobic region and hydrogen-bonding region of amino acids. Designing an antagonist targeting this site might potentially alleviate the effect of ZOL in inhibiting angiogenesis.