Objective To prepare the cleavable PEG and RGD co-modified liposome for tumor targeting.Methods Liposomes were prepared by film-ultrasonic method.The particle size,Zeta potential and stability in FBS were evaluated.Cellular uptake by HepG2 cell was explored.MTT assay was used to evaluate the cytotoxicity of blank liposomes. Results The particle diameter of C/RGD-LP was (104.8 ±5.5 )nm with the Zeta potential of (-4.45 ±1.75 )mV.The cellular uptake of C/RGD-LP increased 2.8 times after Cys was added.The C/RGD-LP showed little cytotoxicity to HepG2 cell.Conclusion Cleavable PEG and RGD co-modified liposomes were easy to prepare and has a special application value for targeting tumor.

Polycystic ovary syndrome (PCOS) is one of the most popular diseases in obstetrics and gynecology research at internal and abroad at present, traditional Chinese medicine(TCM)in the clinical treatment of the disease have the advantage. Clinical epidemiological study of descriptive research method this research adopts investigation, observation of TCM syndromes and improper diet through 401 cases in Jiangsu Province confirmed PCOS patients, to explore the relationship between TCM syndrome type distribution and improper diet factors, and to provide the clinical basis for further etiology of this disease research. TCM syndrome type distribution of the disease is kidney deficiency, phlegm stagnation syndrome, qi stagnation and blood stasis syndrome, syndrome of dampness heat of liver channel and is composed of 4 basic syndromes and formed complex syndrome, and the composite and syndrome type (60.85%); combined with the analysis of traditional Chinese medicine dialectical, Pure empirical syndrome this disease (46.88%), followed by the actual card (45.39%), pure deficiency is rare. Improper diet factors associated with the disease, in which improper diet with different TCM syndrome type distribution significantly related. Stagnation of phlegm dampness syndrome is the main syndrome of the disease type, improper diet factors and every syndrome PCOS type distribution is as follows: the partial eclipse fatness greasy with basic syndromes of phlegm dampness stagnation of kidney deficiency syndrome, the nephrasthenia syndrome is less; eating spicy stimulation by basic syndromes of stagnation of Qi and blood stasis; eating cold people the basic certificate type of qi stagnation and blood stasis; The diet of patients are more prone to stagnation of phlegm dampness syndrome.
Adolescent ; Adult ; China ; Diagnosis, Differential ; Diet ; Eating ; Female ; Humans ; Medicine, Chinese Traditional ; Polycystic Ovary Syndrome ; diagnosis ; metabolism ; physiopathology ; Young Adult

Objective To synthesize 628F-Py-AMD3465,to investigate its biodistribution in mice and to perform the microPET/CT imaging on mice bearing human lung cancer cell (A549).Methods AMD3465 quaternary ammonium salt precursor was directly labeled with 18F,then 628F-Py-AMD3465 was synthesized through nucleophilic reaction,hydrolysis,neutralization and the product was purified using HPLC.The labeling yield and radiochemical purity were analyzed by HPLC.Fifteen Kunming mice were injected with 5.55 MBq of 628F-Py-AMD3465 and sacrificed at 5,20,40,60 and 120 min postinjection.The selected tissues were harvested and weighed,and the radioactivity in the tissues was measured by an automated γ-spectrometer.The ％ID/g was calculated.MicroPET/CT studies were performed on A549-bearing mice after injecting 6-18F-Py-AMD3465 through vena caudal.Paired t test was used.Results 6-18F-Py-AMD3465 was successfully synthesized with the labeling yield of (9.0±2.0)％,the total synthesis time was about 60 min,and the radiochemical purity was more than 98％.Biodistribution studies showed that the radiouptake was higher in the kidneys and bladder of normal mice,which demonstrated that 6-18 F-Py-AMD3465 was mainly excreted through the kidneys.Biodistribution in A549-bearing mice was similar to that in normal mice.The tumor/muscle ratio at 40 min was 5.0,but the radiouptake of the tumor was still lower than that of the normal lung:(8.05±0.35) ％ID/g vs (9.33±0.66) ％ID/g;t=5.26,P＜0.05.MicroPET/CT imaging showed that the high-uptake location of 6-18F-Py-AMD3465 in tumor-bearing mice was similar to the normal mice,and the tumor uptake reached the maximum level at 45 min post-injection (SUV 0.67).Conclusions 6-18F-Py-AMD3465 can be synthesized by a simple method.A lower uptake could be shown in the tumor compared to that in the lung and the tracer has limited diagnostic value for lung cancer.

AIM: To clarify whether advanced glycation end products (AGEs) can influence the expression of mitochondrial fusion proteins Mfn1 and Mfn2 in cultured human aortic endothelial cells (HAECs) in vitro.METHODS:AGE-BSA was used as AGEs.Purchased primary human aortic endothelial cell line was multiplied, and transferred to dif-ferent passages for subsequent grouping.For dose-dependent experiment, HAECs were divided into 4 groups, and the con-centrations of AGE-BSA in each group were 0 mg/L (control group), 50 mg/L, 100 mg/L and 200 mg/L, respectively. For time-dependent experiment, HAECs were divided into 5 groups with the same concentration (100 mg/L) of AGE-BSA, but the intervention time was 0 h (control group), 6 h, 12 h, 24 h and 48 h, respectively.The mRNA and protein expres-sion levels of Mfn1 and Mfn2 in the HAECs were detected by real-time PCR and Western blot, respectively.RESULTS:Exposure of the HAECs to AGEs at different concentrations for 24 h all down-regulated the mRNA and protein expression levels of Mfn1 and Mfn2.Except for 6 h intervention group, 100 mg/L AGEs intervention for 12 h, 24 h and 48 h all down-regulated the mRNA and protein expression levels of Mfn1 and Mfn2 in cultured HAECs.CONCLUSION: AGEs down-regulates the expression of mitochondrial fusion proteins Mfn1 and Mfn2 in cultured HAECs, indicating that AGEs may influence mitochondrial dynamics of human aortic endothelial cells.

ObjectiveTo study the correlation between human erythrocyte membrane phospholipid profile and insulin sensitivity in elderly diabetic patients. MethodsThe levels of phosphatidylcholine (PC), phosphatidylserine(PS),phosphatidtlinostiol(PI),phosphatidylethanolamine(PE),the maximum erythrocyte deformation index(DImax) , the maximum erythrocyte aggregation index(AImax) and glucose disposal contant Ki (KITT) were measured in 32 cases of elderly diabetics and 30 healthy old subjects. ResultsThe KITT was lower in diabetic patients than in normal controls (P

Objective To investigate the effect of propofol on the activation of NF-?B and the expression of Bcl-2 and Caspase-3 gene in cerebral cortex after transient focal cerebral ischemia-reperfusion (I/R) and the possible mechanism. Methods Ninety healthy male Wistar rats aged 3-4 months weighing 250-300g were randomly divided into 3 groups (n=30 each) : group Ⅰ sham operation; group Ⅱ I/R and group Ⅲ propofol + I/R. The animals were anesthetized with intraperitoneal chloral hydrate 300 mg?kg-1. Left common, internal and external carotid arteries (CCA, ICA, ECA) were exposed. Middle cerebral artery occlusion (MCAO) was produced by inserting a nylon thread, 0.26-0.28 mm in diameter and 4.0 cm in length into ICA and advancing it cranially until resistance was felt. After 2 h MCAO the nylon thread was withdrawn to allow reperfusion. In propofol group propofol 100 mg?kg-1 was given IP 10 min before MCAO. The animals were decapitated at 2, 3, 6, 12, 24 and 72 h of reperfusion (n=5 at each time point in each group) . Their brains were immediately removed for determination of translocation of NF-?B in the neurons (by immuno-histochemistry) and expression of NF-?B in cerebral cortex (by Western blotting). The expression of Bcl-2 mRNA and Caspase-3 mRNA in cerebral cortex was determined by in situ hybridization. Neurological deficit was scored and microscopic examination of ischemic cerebral cortex was performed at 24 h of reperfusion. Results In I/R group (Ⅱ) NF-?B was significantly translocated from cytoplasm into the nucleus of the neurons in the ischemic cerebral cortex during 2-24 h of reperfusion while in non-ischemic cortex NF-?B was confined to the cytoplasm. The expression of NF-?B, Bcl-2 mRNA and Caspase-3 mRNA was significantly higher in ischemic cortex than in non-ischemic cortex. Neurologic deficit scores were higher in I/R group than in sham-operation group. Microscopic examination showed congestion and edema of ischemic cerebral cortex and degeneration and necrosis of the neurons in I/R group. In group Ⅲ propofol pretreatment significantly inhibited the translocation of NF-?B, decreased expression of NF-?B and Caspase-3 mRNA and increased Bcl-2 mRNA expression as compared with I/R group (Ⅱ) . Neurologic dificit and histologic damage induced by I/R were significantly ameliorated by propofol pretreatment. Conclusion Propofol pretreatment can inhibit apoptosis of neurons induced by I/R by inhibiting the activation of NF-B, up-regulating Bcl-2 gene and down-regulating Caspase-3 gene.

Objective To investigate the analgesic effect of adenosine A1 receptor agonist R( - )-N6-(2-phenylisopropyl)-adenosine (R-PIA) administered into the brainstem medial pontine reticular formation (mPRF) and the underlying mechanism. Methods Sixty male SD rats aged 8-10 weeks weighing 250-300 g were used in this study. The animals were anesthetized with intraperitoneal 10% chloral hydrate 300 mg?kg-1 .A 24-gauge stainless steel cannula was inserted into mPRF on one side using a stereotaxic apparatus. One week after operation the animals were randomly divided into 12 groups ( n=5 each) : groupⅠcontrol; groupⅡR-PIA 0.5?g; groupⅢR-PIA 1.0?g; groupⅣR-PIA 2.0?g; groupⅤtheophylline (an adenosine receptor antagonist) 5.0?g; groupⅥ8-cyclopentyl-1 ,3-dipropylxanthine (DPCPX, an adenosine A, receptor antagonist) 1.0?g; groupⅦglibenclamide (an ATP-sensitive K+ channel blocker) 5.0?g; groupⅧ4-aminopyridine (4-AP, a voltage dependent K+-channel blocker) 5.0?g; groupⅨtheophylline 5.0?g + R-PIA 2.0?g; groupⅩDPCPX 1.0?g + R-PIA 2.0?g; groupⅪglibenclamide 5.0?g + R-PIA 2.0?g and groupⅫ4-AP 5.0?g + R-PIA 2.0?g. All the drugs were injected into mPRF in 0.3?l of normal saline. In groupⅨ-ⅫR-PIA 2.0?g was administered 15 min after pretreatment with theophylline, DPCPX, glibenclamide or 4-AP. Analgesia was determined using the tailflick latency (TFL) (the time between the onset of the radiant heat stimulus and voluntary tail withdrawal) at 5, 15, 30, 45, 60 and 90 min after R-PIA injection into mPRF. The pain threshold was expressed as percentage of the maximal possible effect ( MPE) : MPE = (TFL after drug - baseline TFL)/( 10.0 -baseline TFL)?100% .Results R-PIA 0.5-2.0?g injected into mPRF produced significant analgesia in a dose-dependent manner. Pretreatment with theophylline or DPCPX completely reversed the analgesic effect of R-PIA while pretreatment with glibenclamide or 4-AP only partially reversed the analgesic effect of R-PIA.Conclusion R-PIA administered into mPRF produces analgesia through activation of both ATP-sensitive and voltage-dependent K+ -channel in mPRF.

Purpose: To confirm the therapeutic effects of thyrotropin-releasing hormone(TRH) on the experimental spinal cord injury. Method: Wistar rats were subjected to incomplete spinal cord injury using the modified Allen method. The effects were observed by means of neurologic scoring, quantitative enzyme histocytoehemistry、quantitative immunohistocytochemistry and electron microscopy. Results: 1) The treated group exhibited significantly higher scores than the control group. 2) Acetylcholinesterase (AchE) activity of anterior horn cells in the treated group was higher than that of the control group invarious time, and its activity restored to normal level two weeks after injury; Acid phosphatase(AePase) activity was lower than that of the control group in various time. and its activity restored to normal level four weeks after injury. The content of Nissl's bodies in anterior horn cells in the treated group was higher than that of the control goup one week after injury. 3)The number of axon in a certain area of spinal white matter in the treated group was more than that of the control group. 4)Ultrastructural observation showed that both the nerve tissue injury and the extent of hemorrhage were milder in the treated group than that of the control group. Conclusion: The therapeutic effects of TRH on the spinal cord injury" are shown not only in the improving recovery of motor function, but also in the morphology.

Objective:To test the validity of the computer-added measure system in pre-clinical practice training of root canal treatment with resin transparent tooth models.Methods:Two groups of students prepared resin transparent tooth models in three ways.Transparent root canal preparation was conducted by the first group, blind root canal preparation and blind followed by transparent preparation were conducted by the second group. Resin transparent tooth models were scanned frontally and laterally before and after the preparation. The computer-added measure system was used to evaluate the effect of instrumentation. The data was analyzed by SPSS 10.0 software.Results:It was helpful to understand the change of root canal shape and the problems in instrumentation by using the computer-added measure system with resin transparent tooth models in pre-clinical practice training. The transparent preparation resulted in lower frequency of the preparation defects(P

Objective To investigate the distribution of ligustrazine hydrochloride in guinea pig blood, cerebrospinal fluid and perilymph fluid afte intramuscular injection. Methods The HPLC was used for determination of ligustrazine hydrochloride in guinea pig blood, cerebrospinal fluid and perilymph fluid afte intramuscular injection by internal and external standard method.Results Ligustrazine hydrochloride could be absorbed into blood rapidly after intramuscular administration in guinea pig. The concentration reach its high level in 20 min.It was 357.76 ?g/ml. It decreased to low level 2 h after injection.It could be found in cerebrospinal fluid 10 min after injection. The concentration reached its high level in 20 min.It was 120.50 ?g/ml.It decreased to low level 70 min after injection. The ligustrazine hydrochloride could be found in perilymph fluid 5 min later.Its high level in 20 min was 215.79 ug/ml.It decreased to low level 70 min after injection.The results indicated that ligustrazine hydrochloride was rapidly absorbed and eliminated after intramuscular administration in guinea pig.Conclusion Ligustrazine hydrochloride can be absorbed into blood, enter cerebrospinal fluid and perilymph fluid. It can pass through blood-brain barrier and blood-labyrinth barrier. The results indicates that ligustrazine hydrochloride is rapidly absorbed and eliminated after intramuscular administration in guinea pig.