After a brief description of the background and present situation of knowledge service in domestic college and university libraries,the knowledge service model,knowledge service team framework and main knowledge service contents were analyzed with the practice and experiences of knowledge service in our library introduced.

On the basis of the research on the work of subject librarian,this article describes the concrete conceive about constructing the key discipline information service platform in universities,analyzing the practical significance,the practical value and the problems to be dissolved in discipline construction.

Objective To compare the influence of open access journals ( OAJ ) of biomedicine on academic exchanges by empirically analyzing the journals enrolled in the Chinese science citation database-the core (CSCD-C).Methods Multivariate statistical analysis was performed on OAJ and non OAJ in CSCD by using bibliometric and statistical methods,SPSS software and rank-sum test.Results The OAJ were accounted for only 31.63％ of the total enrolled journals,the average ratio of funded papers in OAJ was 72.29％.Statistical journals had high influence in the discipline.The selfcitation rates of clinical medicine OAJ and special medical OAJ were high.The average impact factor and h index in biological OAJ were high.The average impact factor of preventive medicine OAJ was high.The average h index of comprehensive non OAJ was high.Conclusions The distribution of OAJ is uneven among different disciplines.The ratio of funded papers is higher in OAJ than in non OAJ with insignificant differences in discipline influence.

Web impact of 30 foreign biomedical OA journal websites was evaluated using link analysis method.The current situation and existing problems of foreign medical OA Journal websites were discussed combined with evaluation results in order to provide references for the construction of medical OA journal websites in China.

Objective To study the effect of acute lymphoblastic leukemia (ALL) children bone marrow mesenchymal stem cells (MSCs) on the resistance of K562cell atd mechanism in vitro.Method MSCs were obtained from AL children bone marrow after derivation, cultivation and identification.The coculture of MSCs and K562 and K562 suspension were established.Effects of MSCs on the growth of K562 cells were investigated in vivo.The two kinds of cells treated with different concentration of adriamycin (ADM) and the rate of apoptosis was evaluated by flow cytometry.Cell cycle was determined by flow cytometry.RT-PCR was used to detect Bcl-2 and Bax in K562 cells.Result Compared with the cell growth curve of K562 alone, the K562 cell co-cultured with MSCs grew slower and the exponential phase of growth was not obvious.The apoptosis index of the K562 cells co- clutured with MSCs was (9.19 ±0.53)% examined by flow cytometry, and that of the K562 cells alone was 4.00 ± 0.37% respectively( P ＜ 0.05 ).The percentage of cells at G0/G1 phase was (50.2 ± 2.26) % and that at S phase was (37.03 ± 3.50) % in the group of K562 alone, but those of the K562 cells co - cultured with MSCs were (80.95 ± 3.83) % and ( 17.40 ± 1.50)% respectively( P ＜0.05).The result of RT-PCR suggested expression of Bcl-2/Bax of the K562 cell co-cultured with MSCs was higher than K562 alone.Conclusion ALL children MSCs suppressed the growth of K562 cell in vitro.Adhesion made K562 depress sensitive to ADM.The mechanism was perhaps caused by adhesion with MSCs, K562 cell cycle was changed and related to Bcl-2 gene high level expression.

Objective To determine whether the inhibition of paxillin tyrosine residues 31 and tyrosine residues 118 (Pxn Y31 and Pxn Y118) phosphorylation via inhibition of c-Abl kinase will effectively block its downstream effector molecules vessel endothelium-cadherin (VE-cad), and whether Rho/Rho kinase activation which will induce the vascular barrier dysfunction. Methods Ninety healthy male Sprague-Dawley (SD) rats were randomly divided into nine groups (each n =10). Only tracheotomy was undergone in the sham group. Groups of protective ventilation were set at a volume tidal (VT) of 6 mL/kg, a positive end-expiratory pressure (PEEP) of 5 cmH2O (1 cmH2O =0.098 kPa) for 1 hour or 2 hours (namely group PVT 1 h and group PVT 2 h), respectively. Groups of high VT were put on mechanical ventilation (MV) at high VT 30 mL/kg, PEEP 0 for 1 hour or 2 hours (namely group HVT 1 h and group HVT 2 h), respectively. Groups UO126 and AG957 pretreatment were set on MV at HVT for 1 hour or 2 hour respectively, but they were given p42/44 mitogen-activated protein kinase (p42/44MAPK) inhibitor UO1261 mg/kg by intraperitoneal injection or c-Abl kinase inhibitor AG95710 mL/kg by intragastric injection 1 hour before HVT ventilation. All the animals were sacrificed after experiments and specimens of lung tissues and bronchoalveolar lavage fluid (BALF) were harvested. Pulmonary vascular permeability was measured by Evans blue (EB). The levels of tumor necrosis factor-α(TNF-α) in BALF were measured by enzyme linked immunosorbent assay (ELISA). Then the change of lung tissue pathology was observed with light microscope, diffuse alveolar damage system (DAD) score and lung wet/dry ratio (W/D) were estimated. The myeloperoxidase (MPO) activity was measured by colorimetric analysis, phosphorylations of c-Abl Y245, Pxn Y31, Pxn Y118, VE-cad Y658, p42/44MAPK Y202/Y204, myosin light chain (MLC) and myosin-associated phosphatasetype Y696 (MYPT Y696) were determined by Western Blot. Results ① There were no obvious pathological changes in the lung tissue in the sham group and PVT 1 h or 2 h group, and also there were no significant differences in all the parameters between above groups. However, the injury in lung tissue was severe in the HVT groups. In addition, DAD score, lung W/D ratio, EB content, the activity of MPO, and TNF-α in BALF in HVT groups were significantly higher than those in sham group and PVT groups. After pretreatment with AG957 or UO126, all the parameters were significantly decreased as compared with those of groups HVT. ② The levels of phosphorylation of the proteins in lung tissue in HVT groups were increased as compared with those of group sham and groups PVT, especially at 2 hours of MV. However, compared with groups HVT, the level of p-VE-cad Y658 in lung tissue decreased significantly in group AG957 and group UO126 at 2 hours after HVT. However, the levels of all phosphorylated proteins at 2 hours were significantly lowered in the AG957 group compared with those of the HVT group [p-c-Abl Y245 (gray value): 0.29±0.04 vs. 0.42±0.04, p-Pxn Y31 (gray value): 0.51±0.03 vs. 0.70±0.05, p-Pxn Y118 (gray value):0.65±0.04 vs. 0.91±0.04, p-VE-cad Y658 (gray value): 0.77±0.07 vs. 1.32±0.07, p-p42/44MAPK Y202/Y204 (gray value): 0.38±0.06 vs. 0.61±0.03, p-MLC (gray value): 0.37±0.04 vs. 0.77±0.05, p-MYPT Y696 (gray value):0.54±0.05 vs. 0.87±0.06, all P < 0.05]. After pretreatment with UO126, the phosphorylation level of VE-cad in lung tissue at 2 hours was significantly lower than that of HVT group (gray value: 0.74±0.04 vs. 1.32±0.07), and the phosphorylation levels of p42/44MAPK and its downstream effector molecules MLC and MYPT Y696 were also significantly decreased [p-p42/44MAPK Y202/Y204 (gray value): 0.38±0.07 vs. 0.61±0.03, p-MLC (gray value):0.37±0.04 vs. 0.77±0.05, p-MYPT Y696 (gray value): 0.55±0.05 vs. 0.87±0.06, all P < 0.05]. Conclusions Pxn Y31 and Pxn Y118 phosphorylation could be blocked by inhibition of c-Abl kinase, which could strengthen VE-cad at attachment junction and might block formation of Pxn-guanine nucleotide-exchange factor H1 (GEF-H1)-p44/42MAPK signalosome which induce activation local Rho signaling, lead to activation of MLC phosphorylation, actomyosin contraction, and increase endothelial permeability.

In view of current contradiction between information resources sharing and the protection of intellectual property,the author pointed out the need to maintain coordinated de-velopment,and for the relationship between the unity of these two opposites proposed some practical measures to further promote the sharing of resources and the sound development of the equity market.

Objective To investigate whether the inhibition of caveolin-1 (Cav-1) phosphorylation will regulate effectively nuclear factor-erythroid 2-related factor (Nrf2) signal pathway and downstream effector molecules and protest against ventilation induced lung injury (VILI) in an animal model in vivo. Methods Ninety male Sprague-Dawley (SD) rats were randomly divided into nine groups (each n = 10): sham group in which rats did not receive ventilation but received tracheotomy; lung protective ventilation (PV) for 1 hour or 2 hours group; mechanical ventilation (MV) at high volume tidal (VT, 40 mL/kg) for 1 hour or 2 hours group; protein tyrosine kinase inhibitor PP2 or rosiglitazone (Rsg) pretreatment + high VT ventilation for 1 hour or 2 hours groups. The two pretreatment groups were given intraperitoneal injection PP2 15 mg/kg or intragastric administration of Rsg 5 mg/kg 1 hour before ventilation respectively. The rats were sacrificed after model reproduction, and bronchoalveolar lavage fluid (BALF) was collected. Pulmonary vascular permeability was measured by Evans blue (EB). The levels of tumor necrosis factor-α (TNF-α), activator protein-1 (AP-1), nuclear factor-κB (NF-κB), and interleukin-8 (IL-8) in BALF were determined by enzyme linked immunosorbent assay (ELISA). Then the lung tissues were collected, the lung wet/dry ratio (W/D) was calculated, the changes in pathology was observed with light microscope, and myeloperoxidase (MPO) activity was determined by colorimetric analysis. Nrf2 mRNA was determined by reverse transcription-polymerase chain reaction (RT-PCR). The expressions of Cav-1 tyrosine residues 14 phosphorylation (pCav-1-Y14), Cav-1, peroxisome proliferators-activated receptor γ (PPARγ) and claudin-5 as well as Nrf2 in cytoplasm and nucleus were determined by Western Blot. The positive expressions of PPARγ and claudin-5 in lung tissues were assayed with immunohistochemistry staining. Results There were no obvious pathological changes in the lung tissue in sham group and PV groups, and there were no significant differences in all the parameters between the two groups either. However, the injury in lung tissue was severe in the high VT groups in which W/D ratio, EB contents, MPO activity, and TNF-α, AP-1, IL-8, NF-κB levels in BALF as well as the protein expressions of Cav-1 and pCav-1-Y14 were significantly higher than those of sham group and PV groups, and the protein expressions of PPARγ and claudin-5 were significant lower than those of sham group and PV groups with a dose-dependent manner; but Nrf2 expressions in cytoplasm and nucleus did not show a statistical increase. After pretreatment of PP2 or Rsg, W/D ratio, MPO activity, EB contents, TNF-α, AP-1, IL-8, and NF-κB in BALF were significantly decreased as compared with those of high VT group, and RT-PCR showed significant up-regulation of Nrf2 mRNA in lung tissues too. Moreover, there was a statistically significant increase in expressed Nrf2 proteins in nucleus in PP2 or Rsg groups as compared with those of high VT groups [Nrf2 in nucleus (gray value): 0.61±0.06, 0.56±0.06 vs. 0.31±0.02 at 1 hour, 0.38±0.06, 0.43±0.07 vs. 0.22±0.03 at 2 hours; all P < 0.05], but no significant difference was found in the expression of Nrf2 protein in the cytoplasm among all groups. The protein expressions of pCav-1-Y14 in PP2 pretreatment groups were significantly lower than those of high VT groups (gray value: 0.89±0.04 vs. 1.48±0.02 at 1 hour, 0.86±0.02 vs. 1.31±0.01 at 2 hours; both P < 0.05); but expressed PPARγ proteins and expressed claudin-5 proteins in PP2 or Rsg pretreatment groups were significantly higher than those of high VT groups [PPARγ (gray value): 0.34±0.07, 0.42±0.13 vs. 0.17±0.07 at 1 hour, 0.38±0.09, 0.33±0.07 vs. 0.16±0.03 at 2 hours; claudin-5 (gray value): 0.33±0.05, 0.38±0.07 vs. 0.14±0.03 at 1 hour; 0.30±0.06, 0.31±0.04 vs. 0.17±0.04 at 2 hours; all P < 0.05]. Conclusions The inhibition of Cav-1-Y14 phosphorylation can increase the expression of Nrf2 in the nucleus, then result in an increase in the protein expressions of PPARγ and claudin-5 of its effector molecules. This effect can reduce the inflammation and capillary permeability of lung tissue in the model of VILI.

ObjectiveTo determine whether the inhibition of caveolin-1 tyrosine residues 14 (Cav-1-Y14) phosphorylation with protein tyrosine kinase inhibitors (PP2) will upregulate heme oxygenase-1 (HO-1) activity to protect against ventilation induced lung injury in vivo of an animal model.Methods Fifty-four male Sprague-Dawley (SD) rats were randomly divided into nine groups (eachn = 6). Group A served as normal control group, in which rats did not receive ventilation but tracheotomy. Groups B1 and B2 received lung protective ventilation respectively for 1 hour or 2 hours. Groups C1 and C2 received high tidal volume (40 mL/kg) ventilation for 1 hour or 2 hours, respectively. The group D1 or D2 also received high tidal volume ventilation for 1 hour or 2 hour respectively, but they were given PP2 1 hour before high tidal volume ventilation. The groups E1 and E2 also received high tidal volume ventilation respectively for 1 hour or 2 hours, but tyrosine kinase inhibitor PP2 and HO-1 inhibitor zinc protoporphyrinⅨ(ZnPPⅨ) were given to animals 18 hours before high tidal volume ventilation. All the animals were sacrificed after ventilation, and the specimens of lung tissues and bronchoalveolar lavage fluid (BALF) were harvested. Then the changes in pathology of lung tissue was observed, and diffuse alveolar damage scores (DAD) were calculated, myeloperoxidase (MPO) activity was measured by colorimetric analysis, lung wet/dry ratio (W/D) was estimated. The expressions of phosphorylated caveolin-1 (P-Cav-1-Y14), caveolin-1 (Cav-1) and HO-1 were determined by Western Blot. The expressions of high mobility group B1 (HMGB1) and advanced glycation end product receptor (RAGE) in lung tissues were assayed with immunohistochemistry staining. The levels of tumor necrosis factor-α(TNF-α) in BALF were measured by enzyme linked immunosorbent assay (ELISA).Results There was no significant difference in all the parameters between group A and groups B. Compared with group B1, DAD score, W/D ratio, the activity of MPO and the concentration of TNF-α in BALF in group C1 were significantly increased [DAD score:7.97±0.59 vs. 0.55±0.13, W/D ratio: 5.70±1.61 vs. 5.04±0.63, MPO (U/g): 1.82±0.14 vs. 0.77±0.26, TNF-α(ng/L): 370.10±29.61 vs. 54.38±8.18, allP< 0.05], and the injury in ventilation 2 hours group was more serious than that in ventilation 1 hour group. Compared with groups C, all the parameters in groups D were significantly decreased. The parameters in groups E were significantly higher than those in groups A, B, and D, but no significant difference was found as compared with groups C. Compared with groups B, the protein expressions of Cav-1 and P-Cav-1-Y14 (gray value) in groups C were significantly increased (1 hour: 1.49±0.02 vs. 1.26±0.13, 1.34±0.02 vs. 0.87±0.04;2 hours: 1.58±0.02 vs. 1.27±0.27, 1.31±0.01 vs. 0.95±0.02, allP< 0.05), and the expression of HO-1 protein (gray value) was significantly decreased (1 hour: 0.59±0.02 vs. 1.10±0.01, 2 hours: 0.49±0.01 vs. 1.20±0.02, both P< 0.05). No significant difference in Cav-1 protein expression between groups D as well as groups E and groups C. The protein expression of P-Cav-1-Y14 in groups D and E was significantly lower than that in groups C. The protein expression of HO-1 in groups D was significantly higher than that in groups C, but the phenomenon was not found in groups E as compared with groups C. Compared with group A, the positive expression of HMGB1 and RAGE in lung tissue in groups C and E was significantly increased, but no significant difference was found between groups B as well as groups D and group A.Conclusion Cav-1-Y14 phosphorylation is the key factor for ventilator induced lung injury, which can not only lead to a decrease in vascular barrier function, but also inhibit the activity of HO-1 enzyme, thus further aggravates inflammatory injury of the lung as induced by mechanical ventilation.

Background Elevated intraocular pressure leads to the loss of retinal ganglion cells and vigorous reaction of retinal glial cells.The expression of nestin in retinal glial cells secondary to hypertention and its significance are unclear.ObjectiveThis study aim to investigate the expression of nestin in retinal glial cells (RGCs) in ocular hypertention rats.Methods The ocular hypertention models were established by cauterizing the limbus-draining veins in the right eyes of 42 SD rats,and a conjunctival incision in the left eyes of the rats served as the sham group.The intraocular pressure (IOP) was measured with the Tono-Pen XL tonometer.The number of RGCs in the rats with ocular hypertention was counted.The expression of the nestin protein in RGCs was semi-quantitatively analyzed using Western by immunochemistry.Double immunofluorescence was carried out to evaluate the the confocal laser scaning microscope.Results Significant differences were found in the IOP between the model group and the sham group at various time points (P＜0.05).In 1 week to 3 weeks after operation,the number of RGCs significantly declined in the model group compared with the sham group (P＜0.05).Immunochemistry showed that from 2 hours through 1 week after operation,the expression of nestin was gradually enhanced in the model group in comparison with the sham group.Western blot revealed that the expression of the nestin protein reflected a similar tendency to that of immunofluorescence.The increased introcular pressure as manifested by the induced expression of nestin.Immunoelectron microscopy also confirmed the induced expression of nestin especially at their end-feet suggests a potential neuroprotective mechanism in neuronal degeneration.Nestin may be a useful biomarker for retinal injury study.