An analysis of the core value of 38 tertiary hospitals in the country identified the humanistic spirit as the lifeline of their core value, comprising such factors as benevolence,professionalism and innovation. It also found that upholding of such a spirit is in line with medical model reform, with improvement of hospital management system, and with the upgrading of hospital staff's humanistic competence. The author pointed out that the atmosphere building of such spirit is a systematic process, and that such a spirit can only exert its entire potential by identifying the key person(s) of education and the point of force application, and igniting the inherent innovation power.

Objective Co-stimulation cells is a kind of natual killer (NK)-like T cells, which can kill tumor cells.Previous studies show that lupeol , an natural plant extracts , can change the growth of NK cells ,γδT cells and their effects on tumor cells .This study aimed to investigate the effects of lupeol on human co-stimulation cells and colonic cancer cell lines SW 480 . Methods The peripheral blood mononuclear cells ( PBMC) from healthy volunteers were induced in vitro by different cytokines and transferred into Co-simulation cells.After SW480 and Co-stimulation cells were incubated with different concentrations of lupeol for different durations , methyl thiazolyl tetrazolium (MTT) was used to detect the effects of lupeol on co-stimulation cells and colonic cancer cell lines SW480. Lactate dehydrogenase was used to determine the cell-killing activity of Co-simulation cells to colonic cancer lines SW 480 . Results The concentration of lupeol in 0.1-200.0 mg/L promoted the growth of Co-stimulation cells and inhibited the colonic cancer cell lines SW480.When the concentration of lupeol is at 12.5 mg/L, the cell-killing activity of Co-simulation cells to colonic cancer lines SW 480 was enhanced significantly compared with the controls (76%vs 40%, P<0.05). Conclusion Lupeol could promote the prolifera-tion of Co-stimulation cells, inhibit the growth of cancer lines SW480, and strengthen the cytotoxicity of Co-stimulation cells against co-lonic cell lines SW480.

Objective To investigate the treatment effects of dahuang gancao decoction on lung Injury complicated by acute necrotizing pancreatitis and explore its mechanism. Methods 90 Wistar rats were randomly divided into 3 groups, namely sham-operated group (SO), ANP group (ANP), dahuang gancao decoction treatment group (DG). 4% sodium taurocholate was injected into the pancreatic duct to induce ANP. Dahuang gancao decoction(0.25 g/ml) 0.6 ml/100 g weight was gavaged in the DG group, the same volume of normal saline was gavaged in the SO and ANP group, which was repeated 12 h later. After 6 h, 12 h, 24 h, all rats were sacrificed, pancreas and lung tissues were harvested to observe the pathological changes and the pathological changes were scored. IL-6, IL-10, TNF-α levels of serum and lung tissue were measured,and the changes of toll-like receptor 4 (TLR4) expression in lung tissue was determined by immunohistochemical method. Results 12 h after ANP induction, the serum levels of IL-6 in SO, ANP, DG group were (14.4±4.0)pg/ml, (171.4 ±41.3)pg/ml, (156.9 ±34.7)pg/ml; the serum levels of IL-10 were (13.7 ±4.5)pg/ml, (120.5 ±23.7)pg/ml, (148.3 ±44.4)pg/ml; the serum levels of TNF-α were (22.4 ±4.7)pg/ml, (261.3 ±51.4)pg/ml, (235.3 ±45.9)pg/ml; the lung tissue levels of IL-6 were (257.3 ±55.9)pg/ml,(2578.3 ±403.0)pg/ml,(2370.0 ±491.0)pg/ml; the lung tissue levels of IL-10 were (80.8 ±20. 8)pg/g, (642.0 ± 107.3)pg/g, (695.3 ± 151.7) pg/g, the lung tissue levels of TNF-α were (207.6 ±98.6)pg/g, (1769.1 ±635.6) pg/g, (1401.1 ±450.5) pg/g; the pancreas pathological scores were 0, 7.00 ±1.33, 6.30 ± 0.95; the lung pathological scores were 0, 6.30 ± 1.42, 5.60 ± 0.97; the expressions of TLR4in lung tissue were 0.09 ± 0. 03, 0.59 ± 0. 09, 0. 52 ± 0. 08. The values in the ANP and DG groups were significantly higher than those in SO group (P < 0. 01 ); except for IL-10, all values in the DG groups were significantly lower than those in ANP group (P < 0.05); there was a positive association between lung and pancreas scores (r =0.807, P<0.01), and lung score was positively associated with the expression of TLR4(r = 0.519, P < 0.01 ). Conclusions Dahuang ganeao decoction may quickly improve lung injury complivated by ANP. The mechanism may involve inhibiting the expression of TLR4 and down-regulating the expression of IL-6, TNF-α, up-regulating the. Expression of IL-10.

Objective To evaluate the effects of morphine preconditioning-postconditioning on ischemia-reperfusion (I/R) injury in isolated rat hearts. Methods Male SD rats weighing 180-200 g were killed after intraperitoneal injection of heparin 500 U/kg. The hearts were immediately removed and perfused in a Langendorff apparatus with K-H solution gassed with 95%O2-5%CO2 .HR and left ventricular systolic pressure (LVSP) were measured from a fluid-filled latex balloon in the left ventricle. Global myocardial ischemia was induced by interrupting perfusion for 45 min followed by 60 min reperfusion. Forty isolated rat hearts were randomly divided into 5 groups (n = 8 each): group 1 (I/R); group II morphine preconditioning (M1 ); group Ⅲ morphine postconditioning (M2); group IV M1 + M2; group V 5-hydroxydecanoate (5-HD) + M2. Group M1 was perfused with K-H solution containing morphine 3.0 μmol/L for 20 min 30 min before ischemia followed by 10 min normal K-H solution perfusion. Group M2 was perfused with K-H solution containing morphine 3.0 μmol/L for 10 min at the beginning of reperfusion followed by 50 min normal K-H solution perfusion. Group 5-HD + M2 was perfused with K-H solution containing morphine 3.0 μmol/L+ 5-HD 10-4 mmol/L for 10 min at the beginning of reperfusion followed by 50 min normal K-H solution perfusion. Myocardial CK-MB activity was measured and myocardial infarct size (IS/AAR) detennined (by 2,3,5-triphenyl tetrazolium staining) at the end of 60 min reperfusion. Results The preconditioning, postconditioning and combination of preconditioning and postconditioning with morphine 3.0 μmol/L perfusion for 10 min all provided cardio-protective effects in terms of IS/AAR and myocardial activation of CK-MB. Conclusion Although the combination of morphine preconditioning and postconditioning can protect the heart against I/R injury, the effects are similar to those of either of them alone, and the reason may be that either of them alone protects the heart against I/R injury via activating mitoKATP .

Objective To determine whether morphine postconditioning (MP) could protect the heart against ischemia reperfusion (I/R) injury and which specific type(s) of the opioid receptor is involved in the cardioprotective effect produced by hiP. Methods Male SD rots weighing 180-200 g were killed after intraperitoneal heparin 500 U/kg. The hearts were immediately removed and passively perfused in a Langendorff apparatus with K-H solution gassed with 95% O2-5% CO2. HR and left ventricular systolic pressure (LVSP) were measured from a fluid-filled latex balloon in the left ventricle. Global myocardial ischemia was induced by interrupting perfusion for 45 min followed by 60 min reperfusion. The experiment was performed in 3 parts. In Part Ⅰ 32 isolated rat hearts were randomly divided into 4 groups (n = 8 each): group Ⅰ control received no treatment; group Ⅱ ,Ⅲ,Ⅳ were first perfused with K-H solution containing morphine 0.3, 3.0 and 30 μmol/L respectively for 10 min immediately after the end of ischemia followed by 50 min normal K-H solution perfusion. In part Ⅱ,the concentration of morphine in K-H solution which provided the best cardio-protective effects was chosen according to the result of Part Ⅰ , 32 isolated rat hearts were randomly divided into 4 groups ( n = 8 each) : group Ⅰ received no treatment; gvoup Ⅱ,ⅢⅣ were first perfused with K-H solution containing morphine for 5, 10, 20 min respectively immediately after ischemia followed by 50 min peffusion with normal K-H solution. In part Ⅲ,the MP method which provided the best cardio-protective effects was chosen according to the result of Part Ⅱ , 37 isolated rat hearts were randomly divided into 5 groups: group Ⅰ control (n=8);group Ⅱ-Ⅴ were first perfused for 10 min with K-H solution containing morphine (Ⅱ,n = 8)/morphine + naloxone 10 μmol/L(Ⅲ, n = 7)/morphine + nor-binaltorphimine 5 μmol/L (specific κ receptor antagonist, n = 7)/morphine + nalu'indole 5 μmol/L (specific δ receptor antagonist, n = 7) followed by 50 min reperfusion with normal K-H solution. Myocardial CK-MB activity was measured and myocardial infarct size (IS/AAR) determined (by 2,3,5-triphenyl tetrazolium staining) at the end of 60 min reperfusion.Results The postconditioning with morphine 3.0 μmol/L perfusion for 10 min provided the best cardio-protective effects in terms of IS/AAR and myocardial release of CK-MB. Nuloxone completely abolished the cardio-protective effects of MP. Nor-binaltorphimine partly reversed the protective effect of MP, while naltrindole had no effects on MP. Conclusion MP protects the heart against I/R injury via activating κ receptor.

Objective To study the effects of dihydroartemisinin and quinine on plasmodium falciparum gametocytes at early stage. Methods Eleven patients with falciparum malaria who had plasmodium falciparum gametocytes at early stage(PFGe) in bone marrow but no matured plasmodium falciparum gametocytes(PFGm) in bone marrow and peripheral blood were allocated to two groups.Group A(n=6) were administered orally with dihydroartemisinin at a total dosage of 480mg for 7 days and Group B(n=5) with quinine sulfate at a total dosage of 10?500 mg for 7 days.The number of gametocytes in bone marrow and peripheral blood was examined at regular time. Results PFGe in bone marrow disappeared in Group A on 10 th day after the first administration while existed in all the cases of Group B on 10 th day and still in 2 cases on 14 th day.The clearance time for peripheral PFGe was 4.8?0.9 days in Group A and 22.0?5.8 days in Group B. Conclusion Dihydroartemisinin can clear PFGe but quinine shows no this action.

OBJECTIVETo determine the genomic structure of low density lipoprotein receptor related protein 5 (LRP5) gene.

METHODScDNA sequence encoding LRP5 was used to screen genomic clones containing LRP5 gene by computer hybridization approach. By comparing the cDNA sequence of LRP5 with the genomic sequences, the genomic structure of LRP5 was determined, and then it was conformed by amplifying and sequencing the sequences of exons and splicing junction.

RESULTSThe genomic sequence of LRP5 gene was 131.6 kb in length, containing 23 exons and 22 introns. Three single nucleotide polymorphisms were detected within the coding sequences of LRP5 gene, namely A459G in exon 2, C2220T in exon 10 and G4416C in exon 21. Four polymorphic markers, D11S1917, D11S4087, D11S1337 and D11S4178, located in the 5' flank sequence, introns 1, 4, and 13 of the LRP5 gene, respectively.

CONCLUSIONThe characterization of genomic structure of LRP5 gene allows the investigators to detect disease-causing mutation within the gene and further study the function of LRP5 gene.

Base Sequence ; DNA ; chemistry ; genetics ; Exons ; Genes ; genetics ; Humans ; Introns ; LDL-Receptor Related Proteins ; Low Density Lipoprotein Receptor-Related Protein-5 ; Polymorphism, Single Nucleotide ; Receptors, LDL ; genetics ; Sequence Analysis, DNA

OBJECTIVETo investigate the effects of D-galactose (D-gal) on aging of rat marrow mesenchymal stem cells (MSCs) and its mechanism.

METHODSMSCs isolated from young (7 d) SD rats were randomly divided into four groups:control group, 1g/L, 10g/L and 50g/L D-gal treatment groups. In control group MSCs were cultured in DMEM containing 10% FBS for 48 h. In the D-gal treatment groups, MSCs were cultured in DMEM containing 10% FBS with 1g/L, 10g/L or 50g/L D-gal for 48 h. The senescence-associated changes were examined with SA-β-galactosidase (SA-β-gal) staining, the expressions of p53, p21 and p16 were detected by Western blot. The living and apoptotic cells were determined by AO/EB staining. Cell proliferation was detected by MTT assay. SOD activity was measured by xanthine oxidase method, and the MDA content was estimated with thiobarbituric acid (TBA) method.

RESULTSCompared to control group, the number of SA-β-gal positive cells and the expression of p53, p21 and p16 were significantly increased in the 10g/L and 50g/L D-gal treatment groups. The apoptosis rate in 50g/L D-gal group was significantly higher than that in control group (P<0.01). The proliferation of MSCs was decreased in the 10g/L and 50g/L D-gal groups compared to control group (P<0.05). After 10g/L and 50g/L D-gal treatment, SOD activity was significantly decreased (P<0.01), and MDA level was increased (P<0.01).

CONCLUSIONThe aging of MSCs can be induced by 10g/L and 50g/L D-gal, which may be associated with the elevated levels of oxidative stress.

Animals ; Apoptosis ; drug effects ; Cells, Cultured ; Cellular Senescence ; drug effects ; Galactose ; pharmacology ; Male ; Mesenchymal Stromal Cells ; drug effects ; physiology ; Oxidative Stress ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo determine the linkage between Smith-Fineman-Myers syndrome (SFMS) and X-linked nuclear protein(XNP) locus.

METHODSPolymerase chain reaction and denaturing polyacrylamide gel electrophoresis were used to genotype two polymorphic short tandem repeats within XNP gene.

RESULTSOne of the two short tandem repeats was informative in SFMS family from Shandong, China. Recombination between SFMS locus and XNP gene was observed in the SFMS family.

CONCLUSIONXNP gene is not associated with the disease in the SFMS family from Shandong, China. SFMS exhibits locus heterogeneity at molecular level.

Abnormalities, Multiple ; genetics ; Craniofacial Abnormalities ; genetics ; DNA Helicases ; Female ; Genetic Linkage ; Growth Disorders ; genetics ; Humans ; Intellectual Disability ; genetics ; Male ; Muscle Hypotonia ; genetics ; Nuclear Proteins ; genetics ; Pedigree ; Phenotype ; Polymorphism, Genetic ; Recombination, Genetic ; Syndrome ; X Chromosome ; X-linked Nuclear Protein

OBJECTIVETo map the gene responsible for nonsyndromic hearing impairment in a consanguineous family.

METHODSFirstly, X chromosome scanning was used to exclude X chromosome. Secondly, candidate gene analyzing and genome scanning were performed by homozygosity mapping. Then, additional markers flanking the tightly linked marker were tested to confirm linkage and decide the candidate region.

RESULTSThe nonsyndromic hearing impairment of this family was autosomal recessive. Twenty-five known genes were excluded. Autosomal genome scanning indicated that D17S1293 was tightly linked with disease gene. And further study mapped the disease gene to a 5.07 cM interval bounded by D17S1850 and D17S1818.

CONCLUSIONThe disease gene of the family is mapped to a 5.07 cM interval between D17S1850 and D17S1818, which is a new locus of autosomal recessive nonsyndromic hearing impairment.

Chromosome Mapping ; methods ; Chromosomes, Human, Pair 17 ; genetics ; Chromosomes, Human, Pair 18 ; genetics ; Chromosomes, Human, X ; genetics ; Consanguinity ; Family Health ; Female ; Genetic Predisposition to Disease ; genetics ; Hearing Loss, Sensorineural ; genetics ; Humans ; Male ; Microsatellite Repeats ; Pedigree