Objective: To explore the effect of resveratrol on the chemosensitivity of cervical cancer cells and its regulatory mechanism. Methods: Hela/DDP cells were divided into four groups: Hela/DDP group, resveratrol group, CDDP group, and resveratrol+CDDP group. Cell viability and proliferation were detected by CCK-8. Cell cycle and apoptosis were tested by flow cytometry. The expressions of p21, CDK2, cyclinD1, caspase-9, caspase-3, Bcl 2 and Bax were measured by Western blot. Results: The sensitivity of Hela/DDP cells to cisplatin was lower than that of Hela cells (P<0.01). Resveratrol significantly enhanced Hela/DDP cells' sensitivity to cisplatin (P<0.01). The inhibition of CDDP on the proliferation of Hela/DDP cells was increased by resveratrol (P<0.01). The G1 phase arrest of CDDP on Hela/DDP cells was enhanced by resveratrol (P<0.01). The expression of p21 was higher in resveratrol group and CDDP group than in Hela/DDP group, and the expressions of CDK2 and CyclinD1 were lower than in Hela/DDP group (P<0.01). Compared with CDDP group, the expression of p21 in resveratrol+CDDP group was elevated with the decrease in CDK2 and cyclinD1 expressions (P<0.01). The induction of CDDP on the apoptosis of Hela/DDP cells was elevated by resveratrol (P<0.01). The expressions of caspase-3, caspase-9 and Bax were higher in resveratrol group and CDDP group than in Hela/DDP group, and the expression of Bcl-2 was lower than in Hela/DDP group (P<0.01). Compared with CDDP group, apoptosis in resveratrol+CDDP group was increased with the reduced expression of Bcl-2 (P<0.01). Conclusion: Resveratrol enhances the chemosensitivity of cervical cancer cells by inducing cell cycle arrest and apoptosis.

Cardiovascular disease is a severe threat to human health and life. Among many risk factors of cardiovascular disease, genetic or gene-based ones are drawing more and more attention in recent years. Accumulated evidence has demonstrated that the loss or mutation of ataxia telangiectasia mutated (ATM) gene can result in DNA damage repair dysfunctions, telomere shortening, decreased antioxidant capacity, insulin resistance, increased lipid levels, etc., and thus can promote the occurrence of cardiovascular risk factors, such as aging, atherosclerosis and metabolic syndrome. In this review, we discusses the possible mechanisms between ATM gene and cardiovascular risk factors, which could be helpful to the related research and clinical application.
Aging ; Ataxia Telangiectasia Mutated Proteins ; genetics ; Cardiovascular Diseases ; genetics ; DNA Damage ; DNA Repair ; Humans ; Mutation ; Risk Factors

This paper summarized practices and experiences of other countries in coordinated care delivery system building,and described the care delivery systems used in various healthcare fundraising patterns.It is found that most countries have defined duties and service coverage of healthcare institutions at all the levels and measures to ensure rational patient flow.In the end,the paper concluded found experiences of these countries and inspirations for China.

Objective To provide references for building the medical rehabilitation system in China by learning the progress and compliance of rehabilitation departments construction at tertiary hospitals. Methods Comparative and quantitative methods were used for dynamic analysis qualitative interview to learn the index compliance of the hospitals in question in 201 1-2012.Results Compared with 201 1, average days of stay of the rehabilitation departments declined in general,yet with insufficient therapists;introduction of early rehabilitation intervention was but 57.1%,and the functional assessment rate of rehabilitation service was less than satisfactory.Conclusion Lack of manpower,varying levels of medical rehabilitation services,and neglect for functional assessment were found to be the main problems in construction of medical rehabilitation departments for the time being.

A PCR method was used to amplify the sequence encoding the mature peptide of?-mannanase of Bacillus subtilis. The gene was inserted into the Pichia pastoris vector pPIC9K, downstream of?-factor signal peptide sequence. The resultant recombinant plasmid pPIC9K-MAN was lineared by BglII digestion and introduced into the host Pichia pastoris GS115 by PEG method. After screen, the recombinant P. pastoris strain MAN22 was obtained and fermented in large scale 5L fermenter. The recombinant mannanase activity could reach to 1102IU/ml. The properties of the recombinant mannanase were characterized.

Objective To investigate the changes of expression of Fas-associated proteins named Fas-associated death domain protein(FADD)and death-associated protein(Daxx)in the ischemic penumbra following transient focal cerebra ischemia in rats.Methods ①Adult male Sprague-Dawley rats were randomly divided into the sham-operated group and the cerebral ischemia model group.Rats underwent right middle cerebral artery occlusion(MCAO)for 2 h and reperfusion for 1,3,6,12 and 24 h using an intraluminal suture technique.The expression of FADD and Daxx mRNA and protein were measured with methods of immunohistochemistry.Western blot and reverse transcription-polymerase chain reaction(RT- PCR)respectively were used in the ischemic penumbra of rats.②Double-label fluorescence confocal laser scanning microscopy(CLSM)was performed to monitor FADD and Daxx intracellular location before and after ischemia.Results RT-PCR,Immunohistochemistry,Western blot experiments indicated that a very low level of FADD mRNA and protein were detected in the cerebral cortex of sham rats.The expression level both of FADD mRNA and protein increased significantly at 3 h after reperfusion,peaked at 12 h,then declined markedly at 24 h in the ischemic penumbra of model rats.RT-PCR,Immunohistochemistry indicated that a relatively high level of Daxx mRNA was detected in the cerebral cotex of sham rats.The expression level of Daxx mRNA increased significantly at 3 h after reperfusion and persisted to 24 h at a high level,whose protein had a same change of expression level in the ischemic penumbra of model rats. Immunofluorescence double-staining laser scanning by CLSM showed that the immunoreactivity of FADD was located in cytoplasm,and the intracellular translocation of the immunoreactivity of Daxx from nucleus to cytoplasm was monitored by measuring the green fluorescence after ischemia.Conclusion The transient upregulation of FADD and the persistant high level of expression of Daxx may contribute to neuronal apoptosis following cerebral ischemia/reperfusion.

The correct pairing of disulfide bonds maintains the correct folding mode and high-level structure formation of peptides and protein drugs, which is crucial for the quality control of products. In order to ensure that the disulfide bonds are correctly paired, disulfide bond analysis is an essential part of peptides and protein drug characterization. Mass spectrometry can be used to analyze disulfide bonds. However, insulin and its analogues have two pairs of disulfide bonds without restriction enzyme cutting site. Conventional collision-induced dissociation (CID) and high-energy induced cleavage (HCD) cannot accurately locate the complex disulfide bond. In our study, three methods were used to localize the complex disulfide, including enzyme digestion combined with key peptide fragment in source decay (ISD) fragmentation method, enzyme digestion combined with partial reduction alkylation method, intact protein source ISD and electron transfer dissociation (ETD) cleavage method, The applicability of insulin aspart, insulin lispro and insulin glargine were also investigated. This study provides a new way for the quality control of disulfide bonding mode of insulin and its analogues, and also provides a reference for the disulfide bond localization of peptides or proteins containing this complex disulfide bond.

Actins ; metabolism ; Bone Neoplasms ; blood ; complications ; diagnostic imaging ; pathology ; surgery ; Diagnosis, Differential ; Female ; Humans ; Hypophosphatemia ; blood ; etiology ; Ilium ; Mesenchymoma ; blood ; complications ; diagnostic imaging ; pathology ; surgery ; Middle Aged ; Osteomalacia ; blood ; etiology ; Phosphates ; blood ; Platelet Endothelial Cell Adhesion Molecule-1 ; metabolism ; Tomography, X-Ray Computed

Qigui Tongfeng tablet (QLTFT) is a traditional Chinese medicine with good effect for treating gout. Here, network pharmacology method and molecular similarity analysis were utilized to study the effective substance basis and molecular mechanism of the QLTFT on the gout. The similarity to the medicinal compounds is reflected in the Tanimoto coefficient that gives the structural similarity of two compounds. Operationally, similar modifiers were described as pairs of concepts with a similarity score of 0. 500. The results of the molecular similarity analysis suggested that the flavonoids in QLTFT could be new leads for gout. Furthermore, complex biological systems may be represented and analyzed as computable networks. Two important properties of a network were degree and betweenness. Nodes with high degree or high betweenness may play important roles in the overall composition of a network. And the results of network analysis showed that dongbeinine, verticinone-N-oxide, verticine N-oxide, peimine, peiminine, isobaimonidine, dongbeirine, peimisine and simi-arenol which with high degree acted on xanthine dehydrogenase/oxidase, matrix metalloproteinase-9, an arachidonate 5-lipoxygenase-activating protein, tyrosine-protein kinase and etc. Inhibition of these targets can prevent the formation of uric acid, reduce inflammation by uric acid and regulate the body's immune response. Thus, these compounds may be the main effective substance basis. The research results not only reveals its molecular mechanism, but also provide a theoretical basis for the quality control of drugs and clinical application.
Gout ; drug therapy ; Humans ; Medicine, Chinese Traditional ; Pharmacology ; methods ; Tablets ; Technology, Pharmaceutical ; methods

To clarify the active components in Guizhi Fuling capsule in treatment of intrinsic dysmenorrhea, pelvic inflammation and hysteromyoma, main components were gradually knocked out from the capsules, the effects of knockout capsules on uterine contraction, TNF-α secretion, murine splenocytes (SPL) and hysteromyoma cells proliferation were evaluated, respectively. The inhibition of capsules on uterine contraction was weakened by gradient knockout of paeoniflorin, paeonol, and amygdalin. The suppression of capsulte on TNF-α secretion was reduced by gradient knockout of gallic acid, cinnamaldehyde, pentagalloylglucose, and pachyman. The promotion of SPL cells proliferation was reversed by gradient knockout of gallic acid, paeoniflorin, cinnamaldehyde, quercetin, and pachyman. The depression of capsules on hysteromyoma cells proliferation was attenuated by gradient knockout of paeoniflorin, paeonol, pentagalloylglucose, and albiflorin. In conclusion, the compounds mentioned-above could be the key active basis of Guizhi Fuling capsule in treatment of intrinsic dysmenorrhea, pelvic inflammation and hysteromyoma.
Animals ; Capsules ; administration & dosage ; chemistry ; Cell Proliferation ; drug effects ; Drugs, Chinese Herbal ; administration & dosage ; chemistry ; Dysmenorrhea ; drug therapy ; metabolism ; physiopathology ; Female ; Humans ; Mice ; Mice, Inbred BALB C ; Molecular Imprinting ; methods ; Tumor Necrosis Factor-alpha ; metabolism