Objective To study the toxicity of herbicide,butachlor,to myocardium of Bufo bufo gargarizans. Methods One hundred and sixty Bufo bufo gargarizans were randomly divided into control group,paddy goup,5 times paddy group,10 times paddy group,forty in each group and the exposure was conducted in the experimental containers at the concentrations of 1,5,10 times of the application dosages( 5,10,30 ml/L) ,1/2 of the body of Bufo bufo gargarizans was immersed in the sulotion. After 3,6,9 days of exposure,electrocardiogram was recorded using calculator living creature signal analysis system and the structures of atrium muscle and ventricles muscle were observed with HE stain. Results The structure of myocardial cells of Bufo bufo gargarizans was damaged by butachlor with different levels. Pathological examination showed that the myocardial cells appeared necrosis in different degrees with the increasing doses of butachlor. Butachlor could affact the eletrocardiogram of Bufo bufo gargarizans with obvious dose-time-dependent manner,time-dependent manner was even dominant. Abnormal electrocardiogram was seen,P-R and Q-T changed. Conclusion Butachlor exposure can damage the structure and eletrocardiogram of myocardial cell in Bufo bufo gargarizans.

Objective Lysine-specific demethylase 1 (LSD1) is a flavin adenine dinucleotide-dependent oxidase, which participates in many biological processes , such as cell proliferation and differentiation and gene activation and repression .The aim of this study was to investigate LSD1 acetylation by histone deacetylase inhib -itor trichostatin A ( TSA) and its effect on TSA-induced apoptosis of ovarian cancer cells . Methods LSD1 shRNA was synthesized and implanted into the pLKO-Tet-On lentiviral vector , which was transfected into HO8910 and SKOV3 ovarian cancer cell lines , and then the transfected cells were screened with 1.5μg/mL puromycin for one week until stable clones were established .The cells were treated for 48 hours with methanol (2 mg/mL, control), TSA (200 nmol/L), TCP (100μmol/L), or TSA+TCP.And in the experiment of RNA interfering the LSD1 expression, the cells were also treated for 48 hours with methanol (2 mg/mL, control), TSA (200 nmol/L), Dox (100 ng/mL), or TSA +Dox.The levels of LSD1 acetylation and its substrate histone H3 lysine 4 dimethylation (H3K4me2) were de-tected by immunoprecipitation (IP) and Western blot.The apoptosis of the cells was determined by Annexin Ⅴ/PI staining and flow cytometry, the transcription levels of the Bax and p21 genes detected by real-time quantitative PCR, and the H3K4me2levels in the promoter regions of Bax and p21 measured by chromatin immunoprecipitation ( ChIP ) .Results In comparison with the methanol control, the TSA group showed significantly increased levels of LSD 1 acetylation in the HO8910(1.00±0.29 vs 5.83±0.46, P<0.01) and SKOV3 cells ( 1.00±0.24 vs 5.07±0.35, P<0.01) as well as that of H3K4me2 ( P<0.01);the total apoptosis rates of HO 8910 and SKOV3 cells were remarkably increased in the TSA, TCP, and TSA+TCP groups (P<0.05), even more significantly in the TSA+TCP than in the TSA and TCP groups ( P<0.05) .The mRNA expressions of Bax and p21 in the HO8910 cells were markedly upregulated in the TSA, Dox, and TSA+Dox groups (P<0.05), even more significantly in the latter than in the former two groups (P<0.05).The TSA group exhibited a higher level of H 3K4me2 than the methanol control in the promoters of Bax(2 .92±0.26 vs 0.68±0.19, P<0.01) and p21 (3.07±0.29 vs 0.93±0.17, P<0.01). Conclusion TSA induces the LSD1 acetylation, while suppression of LSD1 expres-sion and activity may enhance the antitumor activity of TSA .

Objective To evaluate right atrial function in patients with idiopathic dilated cardiomyopathy (IDCM) and ischemic cardiomyopathy (ICM) by using two-dimensional speckle tracking imaging (2D-STI).Methods Study population consisted of 31 patients with IDCM,30 with ICM and 30 healthy subjects.High frame rate two-dimensional images were recorded from the apical four chamber view.Right atrial global longitudinal strain (GLS) was measured using two-dimensional strain soft ware.Results Compared with the controls,left ventricular ejection fraction (LVEF),tricuspid annular plane systolic excursion (TAPSE),right ventricular fractional area change (RVFAC),right ventricular fractional shortening (RVFS) and tricuspid annular peak systolic velocity(S') decreased (P ＜0.05),while right ventricular myocardial performance index (MPI) increased in IDCM and ICM group.There were no significant differences for all above echocardiographic parameters between IDCM and ICM patients.Compared with the controls,right atrial GLS decreased significantly in patients with IDCM and ICM,even much lower in patients with IDCM (P ＜0.001).Conclusions Measurement of right atrial strain using 2DSTI could be used for the assessment of right atrial dysfunction in patients with ICDM and ICM.

Objective Protein arginine methyltransferase 5 (PRMT5),a member of the histone arginine methylation transferase family,is involved in a wide range of biological regulation through ei-ther epigenetic or posttranslational methylation modifications. The pur-pose of the present study was to investigate the effects of PRMT5 on cell proliferation of ovarian cancer cell HO8910. Methods Cell lines HO8910 with PRMT5 overexpression were obtained by transi-ent transfection,which were divided into three groups in the experiment: blank control group (wild-type cell line HO8910),negative control group (HO8910 cells were transfected with pCMV-myc plasmid),and experimental group (HO8910 cells were transfected with pCMV-myc-PRMT5 plasmid). Western blot was used to detect the expression of myc protein,and qRT-PCR was used to detect the ex-pression of PRMT5 mRNA. Cell lines HO8910 with inducible stable knockdown of PRMT5 were established by shRNA interference method,which were divided into four groups: pLKO control group (infected by empty vector lentivirus),pLKO+Dox (100ng/mL) group,shPRMT5 group (infected by PRMT5shRNA lentivirus) and shPRMT5+Dox (100 ng/mL) group. Western blot and qRT-PCR were used to detect the expression of PRMT5 protein and mRNA levels. Dox-induced PRMT5 knockdown was detected by increasing Dox concentration,which includes four groups,Dox 0ng/mL group,Dox 1ng/mL group,Dox 10ng/mL group,Dox 100ng/mL group,and each group was treated for 48 hours. Western blot and qRT-PCR were used to detect the PRMT5 protein and mRNA expression. Colony formation assay,EdU assay,and CCK-8 assay were used to test cells proliferation. The experiment was conducted in two large groups each with two subgroups: PRMT5 knockdown group (Dox-group,Dox+ group),PRMT5 overexpression group (pCMV-myc group,pCMV-myc-PRMT5 group). Western blot was used to detect the effects of PRMT5 expression on proliferation-related proteins. The experiment was conducted in two large groups,PRMT5 knockdown group with four subgroups : Dox 0ng/mL group,Dox 1ng/mL group,Dox 10ng/mL group and Dox 100ng/mL group,and PRMT5 overexpression group with two subgroups (pCMV-myc group and pCMV-myc-PRMT5 group). Results Western blot results showed that the expression of myc was detected in the experimental group in which HO8910 cells were transfected with pCMV-myc-PRMT5,and the expression of PRMT5 mRNA was significantly higher in the experimental group than those in the blank control group and the negative control group (P<0.001) . Western blot and qRT-PCR showed that PRMT5 protein (0.32±0.25) and mRNA expression levels in shPRMT5+Dox group were significantly lower than those of shPRMT5 group (0.89±0.18) (P<0.05). Western blot and qRT-PCR confirmed that PRMT5 protein (0.21±0.24) and mRNA expres-sion in Dox 10ng/mL group and Dox 100ng/mL group (0.08±0.15) were significantly downregulated compared to Dox 0ng/mL group (1.11±0.15) (P<0.05). Colony formation experiments,EdU experiments,and CCK-8 experiments confirmed that the proliferative ca-pacity of cells in Dox+group was lower than that of Dox-group in PRMT5 knockdown group(P<0.05); while in PRMT5 overexpression group,the proliferative capacity of pCMV-myc-PRMT5 group was significantly higher than that of the pCMV-myc group (P<0.05). Western blot results showed that the protein expression of Cyclin D1 was significantly lower in Dox 100 ng/mL group (0.17±0.06) than that in Dox 0 ng/mL group (1.18±0.18) (P<0.05) and the expression of P21 was significantly increased in PRMT5 knockdown group (P<0.05). In the PRMT5 overexpression group,the protein expression of Cyclin D1 in pCMV-myc-PRMT5 group (3.48± 0.22) was higher than that in pCMV-myc group (0.88±0.15) (P<0.05),while the protein expression of P21 (0.08±0.17) were significantly lower than that of pCMV-myc group (4.12±0.10) (P<0.05). Conclusion PRMT5 plays an important role in the proliferation of ovarian cancer cells. Down-regulation of PRMT5 can inhibit cell proliferation and up-regulation of PRMT5 can pro-mote cell proliferation.

AIM To develop a pharmacological network screening method in predicting the potential target,active ingredients and pathway of Salicornia europaea L.for the treatment of diabetes,and to uncover its underlying multi-component,multi-target,multi-pathway mechanism.METHODS Information about fifteen kinds of bioactive chemical constituents of Salicornia europaea L.acquired from a large amount of literature were used to predict the targets according to PharmMapper Server,and such a prediction was also subjected to the screening of the antidiabetes drug targets approved by FDA in the DrugBank database.The relevant information of potential target and pathway was obtained by MAS 3.0 biomolecule function software.Cytoscape software was used to construct the Salicornia europaea L.ingredients-targets-pathways network.RESULTS Fifteen major active ingredients of Salicornia europaea L.affecting in a total of 86 pathways (VEGF signaling pathway,Fc epsilon RI signaling pathway,T cell receptor signaling pathway,etc),including the 30 particular diabetes-related pathways of MAP2K1,MAPK,GSK3B,AKT,etc.,fully demonstrated the multi-component,multi-target,multi-pathway mechanism of Salicornia europaea L.in the treatment of diabetes and its complications,through regulating immune,lipid metabolism,inflammation,apoptosis and other processes.CONCLUSION Given the new understanding in analyzing the scientific connotation of anti-diabetes effect,and the complex system of Salicornia europaea L.,this paper highlights the direction for the next step in the validation experiment of its target and mechanism.

Objective_To investigate the effect of ginsenoside Rg1 on the spleen structure and function of aging rats and its relative mechanism.Methods_Forty SD rats were randomly divided into normal control group, aging model group (D-galactose 120 mg/kg,qd ×42 d), Rg1 intervention group(D-galactose 120 mg/kg,qd ×42 d and Rg1 20 mg/kg, from day 15th,qd ×28 d) and Rg1 control group.After finishing injections the spleen index was meas-ured, paraffin sections were then made to observe spleen microscopic structure.Senescence-associatedβ-Galactosi-dase( SA-β-Gal) stain was used to detect aging splenocytes.The proliferative capacity of splenocytes stimulated with Concanavalin A (ConA) was measured by CCK-8.The content of IL-2,IL-6 and advanced glycosylation end products(AGEs) was detected by ELISA.The level of ROS was analyzed by flow cytometry(FCM).Malondialde-hyde(MDA), superoxide dismutase (SOD) were detected by enzymatic assay.The expression of senescence-associ-ated protein P53,P21 and RB were detected by Western blot analysis.Results_Comparing the Rg1 intervention group with the aging model group, spleen index, splenic white pulp area proportion, the proliferative capacity of splenocytes were significantly increased (P<0.05);The secretory capability of IL-2 and IL-6, the active content of SOD were obviously increased(P<0.01);The percentage of SA-β-Gal positive splenocytes, the productions of ROS and MDA were significantly decreased (P<0.01);The production of AGEs was decreased (P<0.05);The expressions of P53,P21 and Rb were also significantly down-regulated ( P<0.01) .Conclusions_Ginsenoside Rg1 relieves injure of the spleen in aging rats induced by D-galactose.It is suggested that the mechanism may be Rg1 in-hibiting oxidative stress and down-regulating P53-P21-RB signaling pathway.

Stress cardiomyopathy is an atypical myocardial disease induced by emotional or physical stress, with the characteristic of left ventricular systolic dysfunction, transient imaging and electrocardiogram (ECG) changes. Sudden cardiac death can occur in severe cases. Clinical symptoms are likely to appear on acute myocardial infarction, but the exact pathological mechanism is unclear. In the present study, we perform a systematic review of the literature on the clinical manifestations, epidemiological characteristics, ECG, imaging and laboratory tests of stress cardiomyopathy, in order to provide the values for forensic pathology diagnosis.
Death, Sudden, Cardiac ; Diagnostic Imaging ; Electrocardiography ; Humans ; Myocardial Infarction ; Stress, Psychological ; Takotsubo Cardiomyopathy/physiopathology*

Superoxide Dismutase (SOD)(EC 1.15.1.1)is a metalloenzyme that is found in almost all organisms and catalyzes the dismutation of superoxide anion radical to hydrogen peroxide and molecular oxygen. Three unique and highly compartmentalized mammalian SOD have been biochemically and molecularly characterized to date: Cu, Zn superoxide dismutase (CuZnSOD, SOD1), MnSOD (Manganese Superoxide Dismutase, SOD2)and EC-SOD (Extracellular Superoxide Dismutase, SOD3). Cu, Zn superoxide dismutase (CuZnSOD, SOD1)is a copper and zinc-containing homodimer that is found almost exclusively in intracellular cytoplasmic spaces. CuZnSOD is widely distributed and comprises about 90% of the total SOD. Cytoplasmic and periplasmic SOD exists as dimers,whereas chloroplastic and extracellular enzymes exist as tetramers. Structure supports independent functional evolution in prokaryotes and eukaryotes. CuZnSOD are thought to protect the brain, lungs, and other tissues from oxidative stress. This paper reviewed the gene, molecular and chemical structure and biological function of CuZnSOD.

OBJECTIVETo investigate the incidence and variation of tunnel enlargement after anterior cruciate ligament (ACL) reconstruction.

METHODSACL reconstructions using hamstring tendons were performed in 58 patients (58 knees) in the study. MRI scans were taken in a consistent manner at 1, 3, 6, 12 and 24 months after surgery to measure tibial and femoral tunnel expansion.

RESULTSFemoral tunnel enlargement was observed in 9 knees (9/58, 15.5%); Tibial tunnel enlargement was found in 12 knees (12/58, 20.7%). Of those with enlarged bone tunnels, there was no significant difference of tunnel diameters between 1 and 3 months after surgery (P>0.05). Six, 12 and 24 months postoperatively, the average tunnel diameters were larger than those of 1 or 3 months after surgery (P<0.05), however, no significant difference was found in between the tunnel diameters 6, 12 and 24 months postoperatively either (P>0.05).

CONCLUSIONTunnel expansion mainly occurs during 3 to 6 months after surgery, and it remains basically unchanged between 12 and 24 months postoperatively.

Adolescent ; Adult ; Anterior Cruciate Ligament ; surgery ; Anterior Cruciate Ligament Injuries ; Arthroscopy ; China ; epidemiology ; Female ; Femur ; pathology ; Follow-Up Studies ; Humans ; Incidence ; Male ; Middle Aged ; Postoperative Complications ; epidemiology ; etiology ; pathology ; Reconstructive Surgical Procedures ; adverse effects ; methods ; Retrospective Studies ; Tendons ; transplantation ; Tibia ; pathology ; Time Factors ; Transplantation, Autologous

OBJECTIVETo investigate the effect of HMME-PDT (Hematoporphyrin Monomethyl Ether-Photodynamic therapy) on Hyperplastic scar in the rabbit ear.

METHODSThe acute model of dermal Hyperplastic scar in the rabbit ear was established. 24 scars were randomly divided into 2 groups: the experimental group (n = 12) received HMME-PDT treatment, and the controlled group (n = 12) received no special treatment. Specimens were harvested from scars on postoperative 28 day. Scar hyper plasty and collagen fibers were observed by haematoxylin-eosin staining and Van-Gieson staining respectively. The microvessel density was calculated under microscope.

RESULTSCompared with the controlled group, HMME-PDT treatment in the experimental group reduced scar formation, decreased the microvessel density and prevented excess collagen deposition at the wound site.

CONCLUSIONSHMME-PDT may play a role in inhibiting hyperplastic scar in rabbit ear.

Animals ; Cicatrix, Hypertrophic ; pathology ; therapy ; Ear ; pathology ; Female ; Hematoporphyrins ; pharmacology ; Male ; Photochemotherapy ; Rabbits