Objective: To investigate the anticancer activity of the novel lactosyl-norcantharidin nanoparticles (Lac-NCTD-NPs) in vivo and in vitro. Methods: The MTT method was used to study the cytotoxic effects of Lac-NCTD and Lac-NCTD-NPs on HepG2, SMMC-7721, and SGC-7901 cell lines for 12 and 48 h, respectively, and the inhibitory effects of Gal-FBS; Lac-NCTD accumulated in SMMC-7721 cells was assayed by HPLC; The in vivo anticancer activity was evaluated by the tumor-growth inhibition in H22 tumor bearing mice. Results: The in vitro studies showed that the cytotoxic effects of Lac-NCTD-NPs against HepG2 and SMMC-7721 cells were the most powerful, as well as the IC 50 was the lowest, then Lac-NCTD, and they were inhibited remarkably by Gal-FBS; As for SGC-7901 cell line, the cytotoxic effects of Lac-NCTD-NPs and Lac-NCTD were not stronger than that of NCTD, and Gal-FBS had no influence on them at all; The amount of Lac-NCTD accumulated in SMMC-7721 cells was 3. 89 μg (7.02×10-3 μmol, 1×106 cell) after treatment for 12 h; The results of the antitumor activity in vivo suggested that the inhibitory rate of Lac-NCTD-NPs on tumor weight was 63.9%, which was significantly higher than that of NCTD and Lac-NCTD groups at the same molar concentration. Conclusion: The tumor-growth is inhibited effectively by Lac-NCTD-NPs which may be a kind of novel liver-targeting agents and could strongly inhibit the tumor-growth.

OBJECTIVE: To evaluate the cardiovascular safety of glucagon-like peptide-1 receptor agonists (GLP-1 RA) for diabetes systematically. METHODS: Medline, Embase, ClinicalTrails. gov, Cochrane Liabrary, CBM, and CNKI were retrieved to collect all the randomized controlled trials (RCT) with a duration of at least 24 weeks, comparing a GLP-1 RA with a non-GLP-1 RA agent in type 2 diabetes, and then a Meta-analysis was performed with RevMan5.3 software. RESULTS: Fifty-one RCTs, invovling 26140 individuals with type 2 diabetes, were included in the analysis. The difference in the incidence of major adverse cadiovascular events (MACE) between GLP-1 RA and comparators did not reach statistical significance, and the odds ratio was 0.78 (0.57, 1.08), although a favorable trend was observed; while in comparisons with placebo, the incidence of MACE was significantly decreased and the odds ratio was 0.5 (0.28, 0.87); compared with comparators, a significant decrease of the incidence of all-cause and cardiovascular mortality were detected and the odds ratio were 0.53 (0.27, 0.93) and 0.38 (0.16, 0.90), respectively. As for the cardiovascular risk factors, GLP-1 RA significantly decreased the HbA1c, weight, TG, LDL, SBP, but increased the heart rates. CONCLUSION: GLP-1 RA may have a protective effect on cardiovascular diseases, compared with the comparators, especially compared with placebo.

Objective To observe the protective effects of soluble Nogo-66 receptor (NgR1 )antagonist (sNgR1-Fc) on cortical axons after cortical infarction in rats,and to study the phenomenon and molecular mechanism of its protective effects on and regeneration of axons.Methods The cortical infarction was induced by photochemistry,termed photothrombotic cortical injury (PCI).Fifteen Sprague Dawley rats were randomly divided into three groups:Sham-operated group,PBS (phosphate buffered solution) group,and s-NgR1-Fc group.In PBS group,PBS was injected into the lateral ventricle of rats; and in sNgR1-Fc group,sNgR1-Fc was injected instead of PBS. The ipsilateral cortex with lesion was harvested for histomorphometry and transmission electron microscope observation 7 days after PCI. Proteins including GTP-RhoA,p-JNK,p-c-JUN and p-ATF-2 were detected by Western blot,as well as Total-J and Total-RhoA.Results The cortical infarction in rats was successfully induced by photochemistry.Compared with sham-operated group,the pathological changes in PBS groups were more serious,including extensive edema or disappearance of axoplasm of fiber without medulla sheath involved and extensive thickening or layer derangement in axoplasm of fiber with medulla sheath involved.These changes were improved significantly after sNgR1-Fc treatment.The levels of GTP-RhoA,p-JNK1,p-JNK2,p-c-JUN and p-ATF-2 in the PBS group were significantly higher than those in the sham-operation group ( P ＜ 0.05 ),whereas the levels of Total-RhoA,Total-JNKl and Total-JNK2 were not different significantly between these two groups (P ＞0.05 ).The sNgR1-Fc treatment up-regulated the levels of these proteins ( P ＜ 0.05 ).Conclusions There is pathological change in axon induced by cerebral hypoxia-ischemia for a long period after cortical infarction.The mechanisms may be associated with RhoA/ROCK/JNK/c-Jun signal way,which is activated by ischemia injury and related to the inhibition of regeneration in axon.Our study shows that NgR1-Fc may inhibit this pathway significantly,and then promote the regeneration of axon partially.

Objective To investigate the clinic effect of Linezolid for community acquired methicillin resistant staphylococcus aureus (MRS A) pneumonia. Methods The clinic data of the patient- were collected from the First Affiliated Hospital of Sun Yat-Sen University, in addition, the body temperature and white blood cell counts were obtained as the index of treatment. Results It was proved that Linezolid was effective in treating community acquired MRSA pneumonia and showed well tolerance with few adverse events. Conclusion Linezolid demonstrated good clinical and antibacterial activity but very few adverse reactions in elderly patients with community acquired MRSA pneumonia.

The parts of system automatically detecting the standard 12-synchronous-lead ECG (electrocardiograms) signal based on personal computer is introduced in this paper. The object-oriented programming method is adopted based on Windows System. We put forward methods to analyze QRS complex wave, P wave, T wave and ST fragment. In this paper the techniques such as ECG signal preprocessing, cardio wave parameters detecting and wave pattern cognizing are discussed too. Furthermore we use wavelet transform technique to analyze the wave pattern and get sound effect.
Algorithms ; Electrocardiography ; instrumentation ; methods ; Humans ; Pattern Recognition, Automated ; Signal Processing, Computer-Assisted ; Software

Objective To investigate the variation of biomarker of coagulation, anti-coagulation, fibrinolysis in elderly critical patients and find out whether they are related to the disease severity. Methods Sixty-seven patients were no less than 60 years old. Eligible criteria: coincidence with the diagnostic criteria of systemic inflammatory response syndrome (SIRS) and APACHE Ⅱ score was no less than 10 scores. Blood sample was drawn from the venous for the test of biomarker (APTT, PT, TT, D-D, Fib, AT-Ⅲ , PC, PAI-1). According to the existent status,all the patients were divided into two groups:survival group (43 cases) and death group(24 cases) ,meanwhile,according to the diagnostic criteria of MODSE,all the patients were divided into MODSE group (30 cases) and non-MODSE group (37 cases). Results There were significant differences in APACHE Ⅱ score between MODSE group and non-MODSE group, survival group and death group [(25.83 ± 1.19) scores vs(18.1±20.73) scores and(18.81±0.72) scores vs(26.50 ± 1.42) scores](P <0.01). The PT and D-D in MODSE group anti death group were higher than those in non-MODSE group and survival group, the differences were significant (P <0.05),while the activity of AT-Ⅲand PC in MODSE group and death group were lower than those in non-MODSE group and survival group, the differences were significant (P <0.05). The PT,D-D and PAI-1 were positively correlated to APACHE Ⅱ score (related coefficients were 0.328, 0.308, 0.335,P <0.05). The AT-Ⅲ and PC were negatively correlated to APACHE Ⅱ score (related coefficients were -0.469, -0.559,P <0.01). Conclusions The abnormality of eoagnlation-fibfinolysis system exists in elderly critical patients. The extended PT, elevated D-D and PAI-1 ,descended PC and AT-Ⅲ are the hints of disease severity and poor prognosis.

OBJECTIVE: To analyze the rate of 235delC mutation in GJB2 gene in patients with idiopathic sudden hearing loss, and to explore its possible correlation with pathogenesis of idiopathic sudden hearing loss. METHOD: Two hundred and thirty-four patients with diagnosis of idiopathic sudden hearing loss in otolaryngology department were recruited as experimental group. Eighty people with normal hearing level were enrolled as control group. Their peripheral blood samples were obtained and genomic DNA was extracted. Using polymerase chain reaction, the coding region of GJB2 gene was amplified, and 235delC mutation is screened for in GJB2 gene by restriction endonuclease. At same time the clinical data of 234 patients was collected to analyze. RESULT: In 234 cases of idiopathic sudden hearing loss, 5 cases were found to have heterozygous 235delC mutation, none of them harbored homozygous 235delC mutation, the 235delC mutation rate was 2.1% (5/234). No 235delC mutation was found in control group. The rate of 235delC mutation in two group showed no statistically significant difference (P > 0.05). CONCLUSION This research shows that the rate of 235delC mutation in GJB2 is low in patients with idiopathic sudden hearing loss, and suggest that 235delC mutation possible has no correlation with idiopathic sudden hearing loss.
Adolescent ; Adult ; Aged ; Child ; Connexin 26 ; Connexins ; genetics ; DNA Mutational Analysis ; Female ; Hearing Loss, Sudden ; genetics ; Humans ; Male ; Middle Aged ; Mutation ; Young Adult

Objective To study the effect of neuronal Nogo-66 receptor (NgR1) antagonist,soluble Nogo-66 receptor (sNgR1-Fc),on promoting the endogenous neural precursor cells (NPCs) differentiating into neurons in order to clarify the mechanism.Methods The cortical infarction was induced by photochemistry,named photothrombotic cortical injury (PCI).Twelve Sprague Dawley rats were randomly divided (random number) into three groups:Sham-operated group,PBS group,and sNgR1-Fc group.PBS (PBS group) or sNgR1-Fc (sNgR1-Fc group) was injected into the lateral ventricle of brain with a minipump.BrdU (Bromodeoxyuridine) was injected into the peritoneal cavity 4-6 days after PCI.The subdentate gyrus zone (SGZ) of brain from sacrificed rat was harvested for Immunohistochemistry to observe the ratio of NeuN +/BrdU + cells 35 days after PCI.Proteins including Nestin、Notch1 and Mash1 were detected by Western Blot.Results The cortical infarction in rat was successfully induced by photochemistry.Thirty-five days after PCI,the BrdU + cells number and theratio of NeuN +/BrdU + in the SGZ of the ipsilateral cerebrum hemisphere with PCI were significantly higher in sNgR1-Fc group than those in PBS group (P ＜ 0.05).The levels of Notch1,Mash1 and Neuro D in the sNgR1-Fc group were significantly higher than those in the PBS group (P ＜ 0.05),which were significantly higher than those in the Sham-operated group.Conclusions sNgR1-Fc could promote the endogenous NPCs differentiating into neurons in a cortical infarction model.The mechanisms may be attributed to the Notch/bHLH (proneural basic helix-loop-helix genes) signaling way.

0.05) between two groups. Abdominal distention and diarrhea occurred in 6 patients in observed group. Nitrogen balance, PA, TFN, IgA, IgG and IgM after nutritional support were better than those before nutritional support in two groups. Nitrogen balance, PA, TFN, IgA, IgG and IgM were better in observed group than those in the control group. Conclusions:Early nutritional support can improve metabolic status,the immune function and the nitrogen balance in brain operation patients.

Objective To explore the mechanism of Zibu Piyin Recipe (ZBPYR) on spleen yin deficiency diabetes-associated cognitive disorder (DACD). Methods The rats were randomly divided into control group, diabetes mellitus (DM) group, spleen yin deficiency group, spleen yin deficiency DM group and spleen yin deficiency DM+ZBPYR group (treatment group). Type 2 DM models were established by high-fat food feeding and low dose STZ intraperitoneal injection for 4 weeks. Then the classical compound method was used to construct spleen yin deficiency rat models by improper diet, over exertion and yin fluids exhaustion. The treatment group was given ZBPYR by gavage for 15 days, and the other groups were given the same amount of normal saline. Then cerebral cortex, hippocampus, stomach and liver were obtained and the changes of protein expression of PDHE1α in them were observed by Western Blot. Results The protein expression of PDHE1αin cortex of DM group and spleen yin deficiency DM group were lower than control group (P<0.05). PDHE1α expression of treatment group in cortex and stomach increased more significantly than spleen yin deficiency DM group (P<0.05). The expression of PDHE1α protein showed no significant difference among all groups in hippocampus and liver. Conclusion ZBPYR improved spleen yin deficiency DACD by regulating PDHE1αin cortex and stomach.