By the presentation of current intranet development and the analysis of misunderstandings and challenges in intranet security,associated with the security product and the hospital practice,a scheme for establishing a controllable and creditable intranet is put forward.

AIM:To investigate the protective effects and mechanism of mesenchymal stem cells on renal tubule cells treated by cisplatin.METHODS:The mesenchymal stem cells(MSCs)were separated from mouse bone marrow.The necrosis and apoptosis rate of renal tubule cells induced by cisplatin were detected by flow cytometry.After co-culture with MSCs,the above changes of renal tubule cells were detected.RESULTS:In co-culture system,the apoptotic rates of renal tubule cell were decreased obviously and the cell number increased obviously.CONCLUSION:The MSCs protect the renal tubule cells from apoptosis induced by cisplatin.This effect may be related with the paracrine effects of MSCs.

The working principle and points for attention of telemedicine consultation vehicles are expatiated,and solutions for regular malfunction are given.

Objective To investigate the expression of angiotensin-converting enzyme 2(ACE2) protein and mRNA in kidney of different age spontaneously hypertensive rats(SHR) and the role of ACE2 in the development of hypertension. Methods Male SHR(n=30) were allocated to 5 groups by age: 1)one-month-old group(S1); 2)two-month-old group(S2); 3)three-month-old group(S3); 4)six-month-old group(S6); 5)nine-month-old group(S9). Sex and age matched Wistar-Kyoto normotensive rats(WKY)served as controls. The expression of ACE2 mRNA in kidney was determined by reverse transcription polymerase chain reaction(RT-PCR). The expression of ACE2 protein in kidney was assessed by immunohistochemistry and computer image analysis. Results 1)An age-dependent increase of SBP was observed in SHR before six months(P0.05). 2)An age-dependent increase of the ACE2 protein and mRNA levels in kidney was observed in both SHR and WKY(P0.05). The ACE2 protein and mRNA levels in kidney were lower in SHR than those in the matched WKY at every corresponding time point(P

Objective To summarize the experience in diagnosis and treatment of rectal injury. Methods The diagnosis and treatment of 40 cases of rectal injury in the recent 6 years were retrospectively analysed. The diagnosis of rectal injury relied on injury history, clinical presentation,anorectal examination , sigmoid coloscopy ,and explorare laparotomy.38 cases treated by surgery ,including rectal repear ,sigmoid colostomy plus drainge ,and resection of injuried segment of rectum.1case treated by non-operation. 1 case died 2h after admittion. Results 39 cases recovered and 1 case died.Conclusions The condition of rectal injury is very complicate.Due attention should be paid to the diagnosis and treatment.

Hospital building intelligentized system is an important part of digital hospital. Innovative theory in technique integration and service idea of "taking sufferers as center" is incarnated by its design and its development direction of current hospital building. The concept and design principle of intelligentized system in hospital architecture construction are discussed; the composing and function of intelligentized system are also expounded; characteristic and application effect of the system in hospital architecture are analyzed.

AIM: To investigate the expression of Smad2 signal protein in peritoneal mesothelial cells and how transforming growth factor ?1 (TGF-?1) affects its expression. METHODS: Rat peritoneal mesothelial cells were cultured in different levels of TGF-?1 (0,1.25,2.5,10 ?g/L) for different time (0,5,15,30,60,120 min). Endogenous Smad2 expression was evaluated by RT-PCR and immunohistochemical assay. The alteration of subcellular location of Smad2 was determined by immunohistochemical assay. RESULTS: TGF-?1 induced Smad2 mRNA expression, which increased at 5 min, peaked at 30 min, and declined to baseline levels by 120 min, in a time-dependent manner. Smad2 mRNA expression induced by TGF-?1 was also in a dose -dependent manner. TGF-?1 induced Smad2 phosphorlylation and nuclear localization in both time-dependent and dose-dependent manner, which was concordant with mRNA expression. Smad2 translocated from cytoplasm to nuclear accumulation in response to TGF-?1, and peaked at 30 min. CONCLUSIONS: Smad2 is present in peritoneal mesothelial cells. TGF-?1 may activate Smad2 expression and translocation to nuclear in a time-dependent and dose-dependent manner. [

Objective To observe the effect of tacrolimus(FK506)in promoting repair of the injured spinal cord pathway after neural stem cell transplantation in rats. Methods A neurysm clip was used to compress the T8 spinal cord segment of SD rats under microscope to establish model of spinal cord injury.The rats were randomly divided into three groups seven days after injury,ie,control group (injection of normal saline at the injury center),transplantation group(injection of neural stem cells,NSCs,at the injury center),FK506 group(injection of NSCs at the injury center plus 7 days of intrapernerve conduction was compared by using the Basso-Beatfle-Bresnahan (BBB) scale,BDA tracing,somatosensory evoked potential(SEP)and motor evoked potentials(MEP)monitoring at 1,2,4 and 8weeks. Results The motor function of the hind limb after injury was recovered in various degrees with time,with the most significant recovery at 4 weeks.The BBB score reached 6,the maximum at 8 weeks.BDA tracing showed that some nerve fibers were found crossing the injured center of the spinal cord one week later in FK506 group and cell transplantation group,that BDA-positive labeled corticospinal tract fibets were seen across the injury site in all groups by the end ofthe eight weeks.In the FKS06 group,the regeneration could be observed even as 1.7 cm away from tlle injury center.SEP latency was significantly shorter in the FK506 group after two weeks(P<0.05)and the MEP latency in the FK506 group was shortened significantly at four weeks compared with the other groups(P<0.05),indicating that the immunosuppressants could promote the recovery of the injured spihal cord,shorten the latency of SEP and MEP，improve SEP at early stage and MEP at late stage．Conclusions Systemic application immuno suppressive agents FK506 plays an important role in neuroprotection and neurotrophy，which promotes the repair of the injured spinal cord after neural stem cell transplantation．

Objective To explore the effect of Numb on tubular epithelial-to-mesenchymal transition (EMT) in rat proximal epithelial cells. Methods NRK52E cells were treated with different concentrations of recombinant human transforming growth factor-β1 (TGF-β1) (0, 1, 5, 10, 15, 20 μg/L) for 48 h or 10 μg/L TGF-β1 for different times (0, 24, 48, 72 h) in vitro. The expressions of E-cadherin, a-smooth muscle actin(α-SMA) and Numb in NRK 52E cells were detected by RT-PCR, Western blot and immunofluorescence staining. Meanwhile Numb siRNA oligo was transfected into NRK 52E cells with lipofectamine before TGF-β1 treatment, then Western blot was applied to detect the protein expression of E-cadherin, α-SMA and Numb in NRK52E cells. Results TGF-β1 could induce EMT in NRK52E cells in dose- and time-dependent manner. During the progress of TGF-β1-induced EMT, the protein expression of Numb in 5, 10, 15, 20 μg/L group was 1.33 folds (P=0.024), 1.39 folds (P=0.035), 1.45 folds (P=0.025), 1.51 folds (P=0.000) respectively as compared to 0 μg/L group. Likewise, the protein and mRNA expression of Numb in 24 h, 48 h, 72 h group was 1.48 folds (P=0.046) and 1.56 folds (P=0.012), 1.54 folds (P=0.011) and 1.82 folds (P=0.008), 1.79 folds (P=0.028) and 1.82 folds (P=0.002) respectively as compared to 0 h group. Moreover, large amount of Numb was accumulated in the cytoplasm. Down-regulation of Numb expression by siRNA transfection did not influence the basal expression of E-cadherin and α-SMA in NRK 52E cells, but attenuated the progression of EMT in NRK52E cells induced by TGF-β1. The up-regulation of α-SMA protein was reduced to 18.1% (P=0.004) while the down-regulation of E-cadherin protein was reversed to 2.19 folds (P=0.004). Conclusion Numb can promote EMT in rat proximal epithelial cells.

Objective To investigate the effect of mild hypothermia on neuroprotection and prognosis prediction of rats with traumatic brain injury (TBI) by dynamically monitoring the somatosensory evoked potentials (SEP) and quantitative electroencephalogram (QEEG).Methods Forty healthy adult male SD rats were randomly divided into four groups according to random number table,ie,normal control group (with no intervention),sham operation group (fenestration only,without drilling),TBI group (fluid percussion was used to produce moderate to severe TBI),and mild hypothemia group (ice blanket was used immediately after TBI for continuous physical cooling and rectal temperature was maintained at 32-35℃ and rewarmed to 37℃ 6 hours after the initiation of cooling),with 10 rats per group.Changes of SEP and QEEG in all groups were monitored at 6,24 hours,and 7 days after TBI.Results (1) Compared with TBI group,the latency of SEP waves (P1 and N1) on the injured side in mild hypothemia group began to shorten at 24 hours(P ＜ 0.05) and were close to that in the sham operation group at 7 days.(2) Except for normal control group and sham operation group,QEEG in TBI group showed decrease of α rhythm,increase of reactivity slow waves,and decrease or disappearance of QEEG relative power spectral values at all time points.In mild hypothermia group,the reactivity slow waves were decreased with a small amount of α wave; QEEG relative power spectral values were increased at 24 hours and 7 days (especially at 24 hours),but werc still lower than those in normal control group (P ＜ 0.05).Conclusion Mild hypothermia exerts neuroprotective effect through reducing SEP latency,raising relative power spectral values of QEEG,and improving the nerve conduction and brain electrical activity of the injured side.