Mesenchymal stem cells (MSCs)have inherent tumor-trophic migratory properties and low immunogenicity,which allow them to serve as vehicles for delivering effective,targeted therapy to tumors.MSC plays an anti-tumor role by releasing some cytokines,which can be strengthened by oncolytic virus,antiangio-genesis agent,tumor necrosis factor guided apoptosis ligand,IL,IFN and pro-drug.In addition,there are some advantages in combination treatment of MSC and others therapies.

The cost accounting plays central role in enhancing financial management in the hospital. With the increasing hospital competition, conventional model of cost accounting is changing, and gradually replaced with a novel model of cost accounting-total cost accounting. With the wide spread of total cost accounting in all hospitals, it is found that the general operation of hospitals is limited by the original HIS information system. EPR system feathered with the advanced data administration and potent function of financial analysis holding promise in adoption and acceptance by hospitals, serving as information collector and analyzer following HIS system.

ObjectiveTo investigate the clinical phenotypes of familial hypercholesterolemia (FH) caused by exon 13 A606T mutation in low deusity lipoprotein receptor.MethodsClinical data of the suffered family were collected and analyzed,as well as measurement of perivascular intima-medial thickness and follow-mediated-dilation function by ultrasonography.ResultsThere were totally 11 sufferers including 4 males and 9 females,aged 8-90 years,with 2 homozygotes and 9 heterozygotes.Among them, one homozygote showed angina pectoris and hematuria,both homozygotes had skin xanthomata.TC,TG,LDL-C and HDL-C were(7.39 ± 1.30) mmol/L,(0.93 ± 0.36) mmol/L,( 11.76 ± 1.10) mmol/L and ( 1.22 ±0.17) mmol/L,respectively.The left/right sided intima-medial thickness of the common,internal,external and bulb carotid artery were ( 1.15 ±0.45) mm/( 1.30 ±0.60) mm,(0.82 ±0.30) mm/( 1.00 -0.66)mm,(0.77 ±0.28) mm/(0.78 ±0.30) mm and ( 1.40 ±0.59) mm/( 1.46 ±0.71 ) mm respectively.The brachial artery flow mediated dilation rate was (4.85 ±4.80)％.Echocardiography revealed 2 patients with cardiac valvular disease and 3 with atrium septum aneurysm. ConclusionFH patients show a variety of phenotypes incuding extraordinary hypercholesterolemia,subcutaneous xanthomata and premature coronary heart disease.

The relationship between M3 cholinergic receptor agonist (carbachol) hyperstimulation-induced pancreatic acinar cellular injury and trypsinogen activation or NF-kappaB activation in rats was studied in vitro. Rat pancreatic acinar cells were isolated, cultured and treated with carbachol, the active protease inhibitor (pefabloc), and NF-kappaB inhibitor (PDTC) in vitro. Intracellular trypsin activity was measured by using a fluorogenic substrate. The cellular injury was evaluated by measuring the leakage of LDH from pancreatic acinar cells. The results showed that as compared with control group, 10(-3) mol/L carbachol induced a significant increase of the intracellular trypsin activity and the leakage of LDH from pancreatic acinar cells. Pretreatment with 2 mmol/L pefabloc could significantly decrease the activity of trypsin and the leakage of LDH from pancreatic acinar cells (P < 0.01) following the treatment with a high concentration of carbachol (10(-3) mol/L) in vitro. The addition of 10(-2) mol/L PDTC didn't result in a significant decrease in the activity of trypsin and the leakage of LDH from pancreatic acinar cells treated with a high concentration of carbachol (10(-3) mol/L) in vitro (P > 0.05). It was concluded that intracellular trypsinogen activation is likely involved in pancreatic acinar cellular injury induced by carbachol hyperstimulation in vitro. NF-kappaB activation may not be involved in pancreatic acinar cellular injury induced by carbachol hyperstimulation in vitro.
Carbachol/*pharmacology ; Cholinergic Agonists/pharmacology ; NF-kappa B/*metabolism ; Pancreas/metabolism ; Pancreas/*pathology ; Rats, Wistar ; Receptor, Muscarinic M3/agonists ; Trypsinogen/*metabolism

Bronchi ; pathology ; Child ; Humans ; Lung Diseases ; complications ; Male ; Pulmonary Emphysema ; congenital

Objective To evaluate the interference of ALP on cTnI assays. Methods One normal mixed plasma sample and 2 abnormal mixed plasma samples with different cTnI levels were prepared, and then divided them into 8 groups respectively. One group was randomly chosen as control while different amounts of ALP were added into the other seven groups. The concentrations of cTnI and ALP in each plasma portion were detected by ACCESS2 (Beckman-Coulter, Inc ) and AXSYM (Abbott Laboratories )separately. The results of the seven tested groups were then compared with those of the control, so as to evaluate whether ALP could interfere with the cTnI assay. Results When the chemiluminescent Access cTnI assay was carried out for detection of normal plasma, the concentration of ALP was up to 3 716 U/L and did not interfere with the test results of cTnI [(0. 04 ±0.01) μg/L] compared with those of the control portion [(0. 04 ± 0. 01 ) μg/L] (t = 0. 40, P ＞ 0. 05 ). Once the concentration of ALP went beyond 917 U/L, the AXSYM cTnI assay results [( 0.08 ± 0. 01 ) μg/L] were higher than those of the normal control ( t =-4. 89, P＜0. 01 ); When the concentration of ALP was up to 3 534 U/L, the test results of abnormal plasma cTnI detected by the Access assay [( 13.41 ±0. 17) μg/L] did not show significant differences from those of the control [(13.48±0.16) μg/L] (t=0. 52,P＞0.05).Conclusions High concentration ofALP did not interfere with the Access cTnI assay or lead to false positive results. However, the high level of ALP( ＞ 917 U/L) could interfere with the AXSYM cTnI assay and cause a false positive result.

Child ; China ; Humans ; Paramyxoviridae Infections ; physiopathology ; Respiratory Tract Infections ; physiopathology ; virology

Objective The purpose of this research is to study the preventive and therapeutic effects of suramin on lipopolysaccharide (LPS)-induced mouse model of acute lung injury and its molecular mechanism.Methods A total of 24 healthy male C57BL/6 mice were randomly divided into two groups: Control group and suramin group.LPS (5 mg/kg, iv) induced acute lung injury model was used in this study.The severity of lung injury was evaluated using haematoxylin-eosin (HE) staining after the injection of LPS for 0, 24 and 72 hours.The expression of TNF-α and IL-6 mRNA levels were also detected by RT-PCR.In vitro, THP-1 cells were stimulated by LPS (100 ng/mL) with saline or suramin pre-treatment.The expressions of p-ERK1/2, p-JNK and p-P38 were analyzed by Western blot at 10 min, 20 min and 30 min after LPS insult.A 2-tailed Student's t test was used to compare difference between two independent groups.Results Compared with the saline group, the lung tissues injury were significantly decreased in the suramin group of 72 hours after the injection of LPS (saline 3.90 ±0.35;suramin 2.50 ±0.12) (t =7.668, P ＜ 0.01).The expressions of TNF-α (saline 8.35 ± 1.63;suramin 4.62 ± 0.70) (t =4.187, P＜0.01) andIL-6 (saline10.53 ± 2.10;suramin5.53±1.10) (t=4.224, P＜0.01) mRNA were also obviously reduced in suramin group after the injection of LPS for 24 hours.The expression levels of pERK1/2, p-JNK and p-P38 were obviously down-regulated by suramin at 10 min, 20 min and 30 min after LPS stimulation.Conclusion Suramin protected LPS-induced acute lung injury through down-regulating the expression of pro-inflammatory factors, which was closely relative to the inhibition of the MAPK pathway.

Objective In order to analyze the research situation,development tendency and deficiencies in the aspects of nursing competency through investigating about 10 kinds of core nursing periodicals published from the year 2009 to 2013 in China.Methods Using bibliometrics methods to analyze the researches about nursing competency in the periodical literature including Chinese Journal of Nursing,Journal of Advanced Study for Nurses,Chinese Journal of Practical Nursing,Chinese Nursing Research,Journal of Nursing Science,Journal of Nursing Administration,Nursing Journal of Chinese People's Liberation Army,Chinese Nursing Management,Shanghai Nursing,Modern Clinical Nursing published from 2009 to 2013.Results There were 215 research papers about nursing competency in periodicals in the past five years,and a quantity of papers increased stably each year.The study contents mainly involved nursing education,training,competency model and standard system based on nursing competency and so on.Conclusions The researches on nursing competency are getting started in China.The quantity is keeping increase and the related research contents become more colorful and deeply than before.

Objective To investigate the relationship between apolipoprotein E ( ApoE ) gene polymorphism and cerebral infarction patients with different gender and etiological typing. Methods A total of 91 patients with cerebral infarction aged≥60 years ( cerebral infarction group) were enrolled. They were divided into either a large artery atherosclerotic (LAA) stroke group (n=37) or a small artery occlusion (SAO) stroke group (n=54) according to the Trial of Org 10172 in acute stroke treatment (TOAST) classification. A total of 105 age-,sex-,and residence-matched healthy subjects were enrolled as controls. A Nested Allele-Specific Multiplex Polymerase Chain Reaction Method was used to detect the ApoE gene polymorphism. The ApoE gene polymorphism of cerebral infarction of different gender and etiological typing were compared. Results ( 1 ) ApoE Genotypes of E2/2, E2/3, E2/4, E3/3, and E3/4 were detected,but the ApoE E4/4 was not detected. (2) There were no significant differences in the frequencies of ApoE genotypes and each gene carrier frequency between the cerebral infarction group and the control group (all P>0. 05). There was significant difference in ApoE genotype frequencies and each gene carrier frequency of the males between the cerebral infarction group and the control group (P<0. 01,P<0. 05). Both the E3/3 genotype frequency (56. 1%) and ε3 carrier frequency (78. 0%) of the cerebral infarction group were lower than the males of the control group ( 79. 2% and 89. 6% respectively );both the E3/4 genotype frequency (31. 7%) and ε4 carrier frequency (15. 9%) were higher than the control group (7. 5% and 3. 8%respectively). There was no significant differences in the ApoE genotype frequency and gene carrier frequency in female participants between the two groups (all P>0. 05). (3) There were no significant differences in the ApoE genotype frequency and gene carrier frequency among the LAA,SAO,and control groups. There was significant difference in the ApoE genotype frequency and gene carrier frequency in males between the LAA group and the control group (P>0. 01);the genotype frequencies of E2/3 and E3/E3 (6. 7% and 46. 7%),ε2,as well as theε3 carrier frequency (3. 3% and 73. 3%) of LAA were lower than those of the control group (13. 2%,79. 2%,6. 6%,and 89. 6%,respectively);the E3/4 genotype frequency andε4 carrier frequency of the LAA subtype were 46. 7% and 23. 3% respectively. They were all higher than 7. 5% and 3. 8% in the control group. However,there were no significant differences in males among the SAO group,the control group,and the 3 groups of females ( the LAA subtype,SAO subtypes,and the control group) (P>0. 05). Conclusion ε4 gene may be a risk factor for LAA in males. The association of ApoE gene polymorphism with cerebral infarction in females is not found.