1.Ethical and Legal Issues in the Compulsory Medical Service of Mental Patient from“Diagnosing Mental Disorder but Actually Not”
Chinese Medical Ethics 2015;(3):364-368
The event of “diagnosing mental disorder but actually not” violates patients′right of informed con-sent and refused to health , showing some problems of “diagnosing mental disorder but actually not” and mandatory admission process and psychiatric judicial authentication , and also have some ethical problems .Therefore, relevant departments should perfect the laws and regulation , establish a hospitalized psychiatric patients appeal , the appeal channels , at the same time , physicians should follow a correct understanding , respect patients rights , disinterest-ed, the ethical principles of self -supervision and also use constraints should be regulated .
3.Dexamethasone Against Temozolomide's Cyto-inhibition on Gliocytoma Cells:An Empirical Study
China Pharmacy 2001;0(10):-
OBJECTIVE:To evaluate the effect of temozolomide(TMZ)in combination with dexamethasone(DXM)on the proliferation of human gliocytoma U251 cells in vitro.METHODS:Human U251 cells were assigned to 1 of the 3 groups: TMZ(10,25,50,100,200,400?mol?L~(-1),respectively)alone or in combination with 40?mol?L~(-1)DXM(TMZ+DXM group)or control group(none drug).After treatment for 72 hours,the cell morphology,cell inhibition ratio,cell cycle and the apoptotic rate were detected.RESULTS:When TMZ concentration was greater than 100?mol?L~(-1)the cell inhibition ratio was higher in TMZ-treated group than in TMZ+DXM-treated group(P
6.Protective effect of edaravone on corneal nerve of rat with experimental diabetic corneal neuropathy
Chinese Journal of Experimental Ophthalmology 2012;30(2):101-105
BackgroundWith the number of diabetics increases,people pay more attention to the diabetic keratopathy.The major mechanism leading to diabetic keratopathy is diabetic corneal neuropathy.So it is significant to observe pathologic mechanism of diabetic corneal neuropathy. Objective To investigate the protective effects of edaravone( a free radical scavenger) on corneal nerve of rats with experimental diabetic corneal neuropathy,then explain the effects of oxidative stress in the pathologic mechanism of diabetic corneal neuropathy. Methods Seventy Sprague-Daxley male rats were taken as experimental subjects and 20 of them were used as normal control group.The remaining 50 were induced to be diabetic mellitus by a single intraperitoneal injection of streptozotocin and divided into 2 groups randomly:edaravone treated group and diabetic control group.In the edaravone treated group,edaravone(0.2 g/L) eye drops were used 3 times a day until the animal was killed.Five rats in each group were sacrificed at 6,8,10 and 12 weeks respectively.Then the corneal sensation,number of corneal nerve fibers,morphology,content of malondialdehyde(MDA) and activity of superoxide dismutase(SOD) in the corneal tissue were detected.ResultsIn the diabetic control group,the corneal sensation and the number of corneal nerve fibers were decreased,the density of neural network for cluster was sparse,the nerve activity was decreased,the content of MDA in the corneal tissue was significantly increased,the activity of SOD in the corneal tissue was significantly decreased (P<0.01 ).Accompany with the course of disease,the above change was obvious day after day.Compared with the diabetic control group,the corneal sensation and the morphological abnormalities in corneal nerve of edaravone group were improved significantly which had the partial branches to the 12th week,the content of MDA in the corneal tissue was significantly decreased,the activity of SOD in the corneal tissue was significantly increased (P<0.01).Conclusions Edaravone can lower diabetic corneal nerve of rats with experimental diabetic corneal neuropathyinjury,Oxidative stress may be a critical pathologic mechanism of diabetic corneal neuropathy.
7.Bacterial Protein Secretion Pathway with SecA as a Motor
Li-Li ZHAO ; Li-Yan YU ;
Microbiology 2008;0(07):-
There are one third of synthesized proteins must be secreted to the cell surface or to the surrounding environment to acquire their native functional state. Most of them are exported by Sec translocase (secretion pathway). Sec translocase consists of a membrane embedded protein-conducting channel, termed SecYEG and a peripherally associated motor domain, the ATPase SecA. The SecDFyajC heterotrimeric membrane protein complex can facilitates protein translocation. SecB is a molecular chaperone that functions in the protein translocation pathway. SecM (secretion monitor) encoded by the 5' region of the secM-secA mRNA, which elongation arrest is required for upregulated expression of SecA. The signal sequence in the N terminus of the nascent peptide is first recognized by the signal recognition particle (SRP). SecB, the Sec-system-specific chaperone, channels the preprotein to the Sec translocation pathway and, ad- ditionally, actively targets the bound precursor to the translocase by its ability to bind SecA. The preprotein-bearing SecA then binds to the membrane, at a high-affinity SecA-binding site, SecYEG, which constitutes a channel for polypeptide movement. Continued translocation requires cycles of ATP hydrolysis bySecA, which is thought to occur in a step-wise fashion with a step of 20~30 amino acid residues.