Cardiomyopathy, Dilated ; complications ; drug therapy ; Female ; Humans ; Mesenteric Artery, Superior ; drug effects ; physiopathology ; Mesenteric Vascular Occlusion ; complications ; drug therapy ; Middle Aged ; Thrombolytic Therapy ; Treatment Outcome

Central Nervous System Diseases ; complications ; virology ; Child ; China ; epidemiology ; Enterovirus ; Enterovirus A, Human ; Female ; Hand, Foot and Mouth Disease ; complications ; epidemiology ; Humans

Aged ; Anemia, Diamond-Blackfan ; complications ; Aza Compounds ; adverse effects ; Female ; Fluoroquinolones ; Humans ; Quinolines ; adverse effects ; Torsades de Pointes ; chemically induced ; complications

OBJECTIVE: To analyze 113 patients with drug-induced liver disease(DILD) so as to clinically validate the international generally-accepted diagnostic criteria.METHODS: 113 DILD cases were reviewed and categorized according to international generally-accepted diagnostic criteria and then graded separately by Maria clinical scale and DDW-J scale to analyze the correlations.RESULTS: 113 out of 822 patients with liver diseases were DILD(13.7%),among whom 17 were of hepatocellular type(15.0%),92 cholestasis type(81.5%) and 4 mixed type(3.5%).Application of Maria clinical scale and DDW-J scale led to different number of DILD cases diagnosed.DILD were mostly induced by antihyperlipidemic drugs and immunosuppressants followed by anticoagulant drugs.CONCLUSION: DDW-J scale,which is more close to clinical diagnostic criteria,contributed to the standardization of the diagnostic criteria of DILD,yet it has its limitations as well.

Objective To investigate the protective effects of felodipine on mRNA levels of endothelial nitricoxide synthase (eNOS) and inducible nitricoxide synthase (iNOS) as well as the level of nitrogen monoxidum (NO) from human umbilical vein endothelial cells (HUVECs) injuryed by oxidized low density lipoprotein (ox-LDL). Methods Isolated HUVECs were divided into blank control group,ox-LDL injury group treated with ox-LDL of different concentrations (6,12.5 and 25 mg/L),and intervention group of felodipine (0.1,1.0 and 10 ?mol/L)+ox-LDL (25 mg/L). Then eNOS and iNOS expressions were measured by real time-polymerase chain reaction and the level of NO in the supernatants of the cultures was assayed by nitrate reductase method. Results The mRNA expressions of eNOS and iNOS in HUVECs and NO level in the supernatants during treatment with different ox-LDL concentrations were higher than those in control group. However,felodipine significantly down-regulated the expression of iNOS in HUVECs injured by ox-LDL and inceased NO generation. Conclusion Felodipine has protective effects on endothelial cells. The mechanism may be related to its lowering the mRNA expression of iNOS induced by low ox-LDL concentration and increasing NO production.

Objective To investigate the protective effect of felodipine on reactive oxygen species (ROS) generation,mRNA level of inflammatory factors such as intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1),in human umbilical vein endothelial cells (HUVECs) injured by oxidized low-density lipoprotein (ox-LDL) so as to explore felodipine's anti-atherosclerosis mechanism independent of its anti-hypertensive effect. Methods Isolated HUVECs were treated with ox-LDL at different concentrations (6,12.5 and 25 mg/L) for 24 hours so that the optimal concentration and time of ox-LDL treatment were selected. Then the cells were incubated with ox-LDL and treated with felodipine at different concentrations (0.1,1 and 10 ?mol/L). Intracellular ROS level was determined by flow cytometry (FCM). Expressions of inflammatory factors ICAM-1 and VCAM-1 were measured by real time-polymerase chain reaction (real time-PCR). Results ROS generation was increased in HUVECs after treatment with different concentrations (6,12.5 and 25 mg/L) of ox-LDL for 24 hours and there was a significant difference at 25 mg/L ox-LDL (P

Antibacterial therapy is a global health issue. The antibiotic resistance is becoming an increasingly serious threat, which caused by misuse and overuse of antibacterial agents combined with the emergence of new resistance mechanism. The resulting infection treatment risk and incidence of the spread of disease, severe cases and deaths are increased in different degrees. With the extensive application of biomaterials and nanotechnology to biomedicine, extensive research has been conducted on antibacterial infection. With the specific physicochemical properties like optical, electric and magnetic and high penetration, inorganic nanomaterials can produce natural antibacterial effect. Nanomedicine can be designed to allow controlled drug release and targeting effect, thus demonstrated better antibacterial efficiency. In this review, the mechanism of antibacterial resistance is described, and the antibacterial infection research on inorganic nanomaterials, as well as nano-drug delivery system including liposomes, nanoparticles, dendrimers and biomimetic nanocarriers are summarized. Nanomaterials and nanotechnology offer promising strategies for the development of new agents that can improve efficacy on antibacterial infections and overcome antibiotic resistance potentially.

Aim To study the effects of cycle arrest and molecular mechanism in human leukemia HL-60 cells induced by diallyl disulfide ( DADS ) . Methods Cell count, colony formation in soft agar experiments and flow cytometry analysis were employed to observe the DADS-induced cell growth inhibition and the effect of cycle arrest in HL-60 cells. The expressions of Chk1/2 and its downstream element in HL-60 cells were detected by Western blot. Results Cell count revealed that population doubling time increased to 35. 03 h and 71. 82 h, respectively, from 19. 14 h in HL-60 cells treated with 60 and 120 μmol·L-1 DADS ( P<0. 05 ) . Colony formation in soft agar experiments showed that colony formation inhibition rate of HL-60 cells exposed to 30, 60, 90 and 120μmol·L-1 DADS increased to 35. 06%, 62. 10%, 93. 79% and 99. 35%, respectively ( P<0. 05 ) . Flow cytometry a-nalysis exhibited that HL-60 cells treated with 60 and 120 μmol · L-1 DADS for 24 h and 48 h arrested in G2/M phase in a concentration-and time-dependent manner ( P <0. 05 ) . Western blot disclosed that the expression of p-Chk1 increased in a time-dependent manner ( P <0. 05 ); however, Chk1, Chk2 and p-Chk2 were not changed in HL-60 cells treated with 60μmol·L-1 DADS (P >0. 05). The expression of Cdc25C, CyclinB1 and CDK1 decreased after treated with 60 μmol·L-1 DADS in a time-dependent manner ( P<0. 05 ) , but the expression of 14-3-3 protein did not change ( P>0. 05 ) . Conclusion DADS can in-hibit the proliferation of HL-60 cells, and induce G2/M arrest through Chk1/Cdc25 C/CyclinB1/CDK1 path-way.

OBJECTIVETo study expression of MMP-2 in relation to microvessel density (MVD) in esophageal carcinoma.

METHODSForty-eight specimens of esophageal carcinoma (Ec) and 17 specimens of grade II + III epithelial dysplasia (Dy) close to the tumor and 12 specimens of normal tissue (Nt) along the incisional margin were examined by S-P immunohistochemical staining with anti-MMP-2 monoclonal antibody. An anti-CD34 monoclonal antibody was used to show MVD.

RESULTSMMP-2 expression in Ec was remarkably higher than that in Dy, which was higher than that in Nt. MMP-2 expression in Ec and Dy was significantly correlated with MVD in the tumor and nearby tissue. MMP-2 expression and MVD in Ec significantly associated with lymph node metastasis.

CONCLUSIONExpression of MMP-2 plays an important role in angiogenesis and lymph node metastasis of esophageal cancer.

Carcinoma, Squamous Cell ; blood supply ; enzymology ; secondary ; Esophageal Neoplasms ; blood supply ; enzymology ; pathology ; Female ; Humans ; Lymphatic Metastasis ; Male ; Matrix Metalloproteinase 2 ; metabolism ; Microcirculation ; enzymology ; pathology ; Middle Aged ; Neovascularization, Pathologic ; enzymology ; pathology

Objective To detect and analyze the mutation of fibroblast growth factor receptor 3(FGFR3) gene among a family with congenital achondroplasia(ACH).Methods Six blood samples of family member in this pedigree were cellected according to the informed consent process for genetic research,and 2 unralted healthy human blood sample were taken as controls.The mutation at nucleotide position 1 138 on FGFR3 gene was detected by using Polymerase chain reaction and single-strand conformation polymorphism(PCR-SSCP)and polyme-rase chain reaction and restriction endonuclease technology(PCR-RFLP) methods.Results Using PCR-SSCP method firstly,only the proband with ACH and his father in this family had the same abnormal band.The amplified products including 1 138 loci on FGFR3 gene further was analyzed by Sfe Ⅰ digestion,3 fragments including 164 bp,109 bp and 55 bp were detected in the proband and his father again,and the other members in the family and 2 controls just showed 164 bp band.It indicated that just 2 patients (proband and his father) showed heterozygous G→A transition mutation at nucleotide position 1 138 on the FGFR3 gene.The amplified products at 1 138 loci was also detected by MspⅠ digestion,just 1 band was observed in all members in this family and 2 controls.It showed that there was no G→C substitution at nucleotide position 1 138.Conclusions The G→A transition mutation at nucleotide position 1 138 in transmembrane domain of FGFR3 gene may be the main cause of achondroplasia in this family.In this pedigree,the proband showed's father a de novo mutation which was transferred to his child again.