Objective To systematically review the relationship between helicobacter pyloric (HP) infection and ischemia stroke. Methods We searched MEDLINE, BIOSIS, VIP, and China Full Text Journal databases to identify the studies that studied the relationship between HP infection and ischemia stroke. All the studies were strictly screened according to the inclusion criteria, and meta-analyses were performed for the included studies using RevMan 4.2 software.Results Eleven case-control studies involving 1 530 patients with ischemia stroke and 1 451 health controls were included. The results of meta-analyses showed that there was a significant difference in the infection ratio of HP between the patients with ischemia stroke and health controls (OR=1.77, 95%CI 1.38 to 2.28, Plt;0.0001), but this difference was not been found after adjusting some related risk factors (1.22, 95%CI 0.93 to 1.59, P=0.15). The results of subgroup meta-analyses showed these differences were only found in the LAA (large-artery atherosclerosis) subgroup (OR=3.65, 95%CI 2.58 to 5.17) and the SAA (small-artery atherosclerosis) subgroup (OR=1.74, 95%CI 1.30 to 2.34), but was not found in the CE (cardiogenic cerebral embolism) subgroup (OR=1.08, 95%CI 0.58 to 2.02). Conclusion HP infection is associated with ischemia stroke, but the relationships between HP infection and the subtypes of ischemia stroke are different. The association between HP and LAA is ber than that between HP and the other subtypes. More evidence is needed to prove whether Helicobacter pyloric infection is an independent risk factor of ischemia stroke.
Objective To study the effect of p38MAPK activity on tumor necrosis factor-α （TNF-α） mRNA and intercellular adhesion molecule 1 （ICAM1） mRNA expressions of isolated rabbit liver during early stage of cold preservation and reperfusion period. Methods Based on the cold preservation and reperfusion model of isolated rabbit liver, the animals were divided into inhibition group （n=12） with 3 μmol/L SB202190 (p38MAPK specificity inhibitor) in perfusate and control group （n=12） with no SB202190 in perfusate. Liver tissue samples were harvested at the time points of before resection, end of cold preservation, and different reperfusion period (10, 30, 60 and 120 min). Protein expression and activity of p38MAPK were detected by Western blot and immunoprecipitation respectively, expression of TNF-α mRNA was detected by RT-PCR, and expression of ICAM1 mRNA was detected by in situ hybridization. Results There was no obvious change of expression of p38MAPK protein in liver tissue both in two groups during the total period （P＞0.05）， and there was no statistically significant difference between two groups （P＞0.05）. At time points of end of cold preservation, 10, 30 and 60 min of reperfusion, the activity of p38MAPK in control group was significantly higher than that at the time points of before resection and 120 min of reperfusion (P＜0.01), and was also significantly higher than that in inhibition group at the same time points (P＜0.01). There was no significant difference in activity of p38MAPK among all time points in inhibition group (P＞0.05). The expressions of TNF-α mRNA and ICAM1 mRNA at the time points of before resection, end of cold preservation, and 10 and 30 min of reperfusion were significantly lower than those in 60 and 120 min of reperfusion in both two groups (P＜0.05, P＜0.01); The expressions of TNF-α mRNA and ICAM1 mRNA in inhibition group were significantly lower than those in control group at the time points of 60 and 120 min of reperfusion (P＜0.01). The activity of p38MAPK of liver tissue during cold preservation and reperfusion period was significantly correlated with the level of TNF-α mRNA and level of ICAM1 mRNA expression （r=0.996, P＜0.01； r=0.985, P＜0.01）. Conclusions These results suggest that p38MAPK pathway may regulate the expressions of TNF-α and ICAM1 at the level of transcription and the activation of p38MAPK can up-regulate TNF-α and ICAM1 expressions, which may be one of the important mechanisms to cause ischemia-reperfusion injury of isolated liver during cold preservation and reperfusion period.
Objectives To investigate the effect of the combined treatment with probiotics and lactulose of gastrointestinal function and postoperative infection after open cardiac surgery.
Methods We retrospectively analyzed the clinical data of 264 patients underwent cardiopulmonary bypass in our hospital between August 2013 and June 2014. There were 129 males and 135 females at the mean age of 53.06±10.97 years. We divided those patients into a treatment group and a control group. In the treatment group, there were 58 males and 63 females at the mean age of 52.29±14.31 years. They took probiotics and lactulose from the first day to the seventh day after operation. In the control group, there were 71 males and 72 females at the mean age of 52.29±14.31 years. They didn’t take probiotics or lactulose after the surgery. Procalcitonin (PCT) and lipopolysaccharides (LPS) concentrations were measured before operation, at 24 hours postoperatively, at 72 hours and on the seventh day. We recorded the condition of postoperative infection, gastrointestinal disorders and relative informations.
Results The PCT and LPS concentrations in the treatment group after 72 hours postoperatively were statistically lower than those of the control group (1.04±5.39 ng/ml vs. 3.51±4.28 ng/ml, P=0.04; 11.28±4.34 EU/ml vs. 21.59±7.34 EU/ml, P=0.03). The PCT and LPS concentrations in the treatment group were also statistically lower than those of the control group on the 7th day postoperatively (0.17±2.79 ng/ml vs. 1.98±4.62 ng/ml，P=0.04; 6.74±6.38 EU/ml vs. 15.96±4.61 EU/ml, P=0.01). The ICU stay time (43.25±14.36 h vs. 63.47±24.46 h, P=0.01) and postoperative hospital stay time (15.07±4.52 d vs. 21.08±6.49 d, P=0.02) were significantly less in the treatment group than those in the control group. The morbidity of infection and the morbidity of gastrointestinal disorders of the treatment group were statistically less than those of the control group (1.65% vs. 5.59%, P=0.00; 2.48% vs. 6.99%, P<0.001), and there was no statistical difference in mortality between the two groups (1.65% vs. 2.10%, P=0.12).
Conclusions The combined treatment with probiotics and lactulose can improve the postoperative inflammatory reaction, gastrointestinal function, and reduce the morbidity of infection.
ObjectiveTo observe the expression of Caspase-3, Caspase-8, Bcl-2, Bax in the rat retina of ocular ischemic syndrome (OIS).
Methods30 Brown Norway rats were randomly divided into experimental group and control group, 15 rats in each group. The rats in experimental group were established a model through ligating the bilateral common carotid artery. At 3 months after modeling, the retinal thickness and ganglion cell (RGC) density were measured by hematoxylin eosin staining; the expression of Caspase 3, Caspase 8, Bax and Bcl-2 in the retina was measured by quantitative real-time reverse transcription polymerase chain reaction.
ResultsThe RGC density in control group and experimental group was 61.97±9.07 and 38.1±5.98, respectively. Compared to the control group, the RGC density was diminished in the experimental group (t=3.059, P < 0.01). A significant decrease was found in the total retina (t=3.036), inner plexiform (t=3.715), inner nuclear (t=3.339) and outer plexiform (t=3.341) thickness (P < 0.05). However, no change of the thickness was evident in the outer nuclear layers (t=2.000, P > 0.05). The levels of protein and RNA expression of Caspase 3, Caspase 8 and Bax in the retina were increased in experimental group (F=17.036, 7.787, 11.431, 11.162, 17.763, 12.183; P < 0.05), while the Bcl-2 expression were decreased (F=10.298, 12.047; P < 0.05).
ConclusionsThere is obvious expression of apoptosis-associated proteins in the rat retina of OIS. Caspase 3, Caspase 8 and Bax expression are increased, while Bcl-2 expression are decreased.
Objective To investigate the effect of cold ischemia on the development of transplant arteriosclerosis (TA) in rat aortic isografts. Methods Aorta grafts from SD and Wister rats were stored in a cold perfusion solution for 0.5 hours and 4 hours respectively before being orthotopically transplanted to Wister recipients. After observation times ranging from 15 to 60 days, the grafts were examined by using histological and electron microscopy techniques. Regional changes in the lumen, intima and media layers were measured by using an image analysis system. Results Partial intima thickings were showed in control isografts at 60 day posttransplantation. Pronounced intima thickings were seen in experimental isografts and control allografts at the same time. The thicking neointimas consist mainly of monocyte/macrophage and smooth muscle cells (SMC). The broken interior elastic lamina (IEL) and necrosis SMC in media were detected in allogenic grafts. Conclusion The damage due to prolonged cold ischemia time is sufficient to cause pronouced graft arteriosclerosis.
ObjectiveTo investigate the effect of power-assisted intravascular shunt in replantation of amputated limbs of rabbits.
MethodsEighty rabbits weighing 1.8-2.5 kg (male or female) were selected to establ ish the model of circular amputation at the hind groin, only femoral arteries and veins were completely preserved. After the femoral artery was clamped in 60 rabbits, the rabbits underwent power-assisted intravascular shunt with high-flow rate (group A, n=20), powerassisted intravascular shunt with low-flow rate (group B, n=20), and no power-assisted intravascular shunt (group C, n=20) to reconstruct blood supply; the femoral artery was not clamped in another 20 rabbits of sham group (group D). Before and after intravascular shunt (1, 3, 6, and 12 hours), the malondialdehyde (MDA), lactate dehydrogenase (LDH), and creatine kinase (CK) of the serum were determined. The myeloperoxidase (MPO), MDA, and wet to dry weight ratio (W/D ratio) of the gastrocnemius muscle were measured, and the thrombogenesis and survival rate of limb were observed.
ResultsBefore intravascular shunt, MDA, LDH, and CK of the serum and MPO, MDA, and W/D ratio of the muscle showed no significant difference among 4 groups (P>0.05). At each time point after intravascular shunt, no significant difference was found in all indexes between groups A and D (P>0.05); the indexes of groups B and C were significantly higher than those of groups A and D (P<0.05); the values were the highest in group C (P<0.05), and reached the peak at 12 hours. All limbs of group A survived with low thrombosis rate, and less limbs could survive with high thrombosis rate in group C.
ConclusionThe power-assisted intravascular shunt with high-flow rate can effective ensure the blood supply of the amputated limbs of rabbits with lower limb injury and higher survival rate of amputated limbs after replantation.
Objective To investigate the research base and current understanding of the mechanism of ischemia-reperfusion injury (IR) to intrahepatic cholangiocytes after l iver transplantation, so as to identify the key points of the mechanism and provide references for cl inical practice. Methods We searched PubMed (1970 to 2007) and CBM(1979 to 2007). Qual ity assessment and data collection were performed by two reviewers independently. Since the baseline supplied and the measure were very different, we decided to provide a descriptive summary only. Results The earliest study on liver IR was publ ished in 1970. A total of 65 papers were included. There were 13 on cl inical studies, 35 on basic research studies; and 17 review articles. Most basic studies focus on injury mechanism: ① The physiology of bile ducts and Intrahepatic Bil iary Duct Cells(IBDC); ②the IR caused injury mechanism of IBDC during or after liver transplantation; ③ the basic injury mechanisms include: cold ischemia, warm ischemia, reperfusion, injury of bile and bile salts. Most clinical studies focused on preventive measures, including surgical and non-surgical approaches. Based on the evidence from basic research, changing the composition and perfusion methods of perfusate and protecting the specific blood supply to biliary ducts and cholangiocytes during the operation were important in preventing or reducing such an injury. Conclusion ① The heterogeneity of morphology, function, status and the special blood supply in large and small IBDC are important material base. ② Our own study indicated that simple IR or H/R was able to change the expression of MHC, MIC, DR4, DR5 and other adhesion molecules. ③ Compared to hepatic cells, hIBDC can’ t resist cold ischemia and even worse in tolerating reperfusion injury. ④ Hydrophobic bile salts will could increase the harm to bile ducts during organ preservation. ⑤ Due to the low quantity and limited quantities of clinical researches, the power of evidence was low. The evaluation indexes and baseline conditions are not unified. So the conclusions are for reference only.
Ocular ischemic syndrome (OIS) is a disease seen in cardiology, ophthalmology, neurology, and neurosurgery, which can lead to brain and ocular symptoms induced by carotid artery obstruction or stenosis. In local and general manifestation, ocular symptoms usually appear first. Ocular symptoms show the prewarning effect of other ischemic damage. Ophthalmologists should pay attention to the clinical manifestation and damages of OIS. The establishment of multidisciplinary diagnosis and treatment patterns for OIS is a pivotal issue for several disciplines.
Objective To investigate the relationship between graded spinal cord ischemia/reperfusion injury and somatosensory evoked potentials(SEP),neurologic function score（NFS）and the histopathological changes of spinal cord. Methods Forty rabbits were randomized and equally divided into 4 groups: shamoperation group, ischemia for 30min, 45min and 60min groups. The spinal cord ischemiareperfusion injury model was created by occlusion of the abdominal aorta in rabbits. SEP was monitored before ischemia,5,10minutes after ischemia, 15, 30 minutes, 1,2, 24 and 48 hours after reperfusion. NFS was evaluated at 6,12,24 and 48 hours after reperfusion.The pathological changes of spinal cord were observed after reperfusion 48 hours. Results The pathological characters with mild,moderate and severe spinal cord ischemia/reperfusion injury could be simulated by declamping after 30， 45 and 60 minutes infrarenal aorta crossclamping. SEP amplitude returned to normal after reperfusion 15 minutes（Pgt;0.05）and SEP latency returned to normal after reperfusion 30 minutes（Pgt;0.05）during mild spinal cord ischemia/reperfusion injury.SEP amplitude returned to normal after reperfusion 30 minutes（Pgt;0.05）and SEP latency returned to normal after reperfusion 60 minutes（Pgt;0.05）during moderate spinal cord ischemia/reperfusion injury. SEP latency increased and SEP amplitude decreased during severe spinal cord ischemia/reperfusion injury,compared with other groups, there were significant differences in SEP latency and SEP amplitude by clamping the infrarenal aorta for 60min（Plt;0.01）. With graded spinal cord ischemia/reperfusion injury, compared with shamoperation group, spinal cord ischemiareperfusion groups had significant differences in NFS（Plt;0.01）. Conclusion SEP is much quicker in the recovery of amplitude than latency during spinal cord ischemia/reperfusion. SEP is a sensitive and accurate index for spinal cord function during ischemia/reperfusion injury. SEP monitoring spinal cord ischemia/reperfusion injury during operation provides experimental basis for clinical application.
ObjectiveTo investigate whether emulsified isoflurane applied after an ischemic episode induces postconditioning in an ischemia model of myocardial injury and its underlying mechanism.
MethodsBetween March and October 2012, using a model of in situ myocardial ischemia and reperfusion injury in rats, cardioprotective effects of emulsified isoflurane were examined by determining infarct size, myocardial damage markers and the concentration of tumor necrosis factor (TNF)-α.
ResultsEmulsified isoflurane postconditioning limited infarct size compared with control groups. It increased serum concentrations of superoxide dismutase while decreased malonaldehyde. TNF-α positive cells were also significantly reduced in emulsified isoflurane group compared with control group. Infusion of intralipid had no effect on infarct size or other variables.
ConclusionIntravenous administration of emulsified isoflurane after reperfusion protects hearts against reperfusion injury, which may be mediated by the inhibition of cardiac damage markers and the concentration of TNF-α.
