[Initial exploration of transfusion-free liver transplantation].

Objective: To evaluate the effect of transfusion-free techniques on the prognosis of liver transplant patients. Methods: The recipients of adult liver transplantation at Tianjin First Central Hospital from August to December 2019 were included in the clinical observation. Liver transplantation without allogeneic blood transfusion was performed through anesthesia management techniques such as acute hemodilution or phlebotomy without volume replacement,maintaining decreased baseline central venous pressure and cell saver. According to the actual results,the patients were divided into two groups: transfusion-free group(n=21) and allogeneic transfusion group(n=28). There were 13 males and 8 females aged of (56.3±11.6) years in the transfusion-free group;and there were 16 males and 12 females aged (54.3±14.2)years in the allogeneic transfusion group. The transplant recipients who had not adopted transfusion management strategy from January to July 2019 were included as control group(27 males and 13 females,aged of (58.9±14.1)years). The clinical data of patients in perioperative period were collected to compare whether there were differences in the recovery of liver function and early complications among the three groups, one-way ANOVA test, rank-sum test, and χ2 test were used for data analysis. Results: The amount of intraoperative blood loss in both the transfusion-free group and the transfusion group was less than that in the control group((454.2±271.3)ml vs.(673.6±333.4)ml vs.(890.3±346.7)ml;q=-6.342,-5.286,both P<0.05).The duration of stay in ICU of the transfusion-free group was less than that of the transfusion group and control group((36.4±9.1)hours vs.(44.3±14.9)hours vs.(58.2±21.1)hours;q=-4.432,-3.824,both P<0.05).The mean ALT level at 7 days after operation was significantly lower in the transfusion-free group than in the control group((56.8±32.1)U/L vs.(89.6±45.6)U/L;q=-3.358,P<0.05). Conclusions: The improvement of multi-disciplinary transfusion management technology aimed at transfusion-free liver transplantation can effectively reduce intraoperative hemorrhage and help to avoid surgical transfusion. Transfusion-free liver transplantation is beneficial to the early postoperative recovery,and its long-term clinical significance is worthy of further clinical research.

Influence of COL1A2 gene variants on the incidence of hypertensive intracerebral hemorrhage in a Chinese population.

Type I collagen (transcribed by COL1A1 and COL1A2 genes) is important for maintaining vessel wall elasticity and is a critical part of the extracellular matrix. We conducted a case-control study to investigate the role of the COL1A2 rs42524 polymorphism in the development of hypertensive intracerebral hemorrhage. Between January 2012 and December 2014, a total of 227 patients with hypertensive intracerebral hemorrhage and 227 controls were selected from the Affiliated Hospital of Yanan University (China). Genotyping of the COL1A2 rs42524 polymorphism was performed using polymerase chain reaction coupled with restriction fragment length polymorphism. By logistic regression analysis, we found that the CC genotype was associated with increased risk of hypertensive intracerebral hemorrhage as compared to the GG genotype (OR = 12.67, 95%CI = 3.03-112.11). In a dominant model, the GC + CC genotype of the COL1A2 rs42524 polymorphism was associated with a 2.57-fold increased risk of hypertensive intracerebral hemorrhage as compared to the GG genotype. In a recessive model, the CC genotype of the COL1A2 rs42524 polymorphism was correlated with a higher risk of hypertensive intracerebral hemorrhage as compared to the GG + GC genotype (OR = 12.07, 95%CI = 2.89-106.75). The GC and CC genotypes of the COL1A2 rs42524 polymorphism were associated with a substantial risk of hypertensive intracerebral hemorrhage among patients who consumed alcohol and used tobacco. In conclusion, our study suggests that the COL1A2 rs42524 polymorphism is associated with the development of hypertensive intracerebral hemorrhage, particularly in conjunction with tobacco use and alcohol consumption.

Repair of spinal cord injury in rats by umbilical cord mesenchymal stem cells through P38MAPK signaling pathway.

OBJECTIVE: To explore the repair of spinal cord injury (SCI) in rats by umbilical cord mesenchymal stem cells (UCMSCs) through the p38mitogen-activated protein kinase (MAPK) signaling pathway. MATERIALS AND METHODS: A total of 45 healthy adult male Sprague-Dawley rats weighing 180-220 g and aged 6-8 weeks old were randomly divided into group A (SCI model + transplantation of UCMSCs, n=15), group B (sham operation), and group C (SCI model + injection of an equal dose of DMEM, n=15) using a random number table. The morphology of spinal cord tissues was observed via hematoxylin-eosin (HE) staining, and the protein expression of phosphorylated p38 (p-p38) in spinal cord tissues, the expression of glial fibrillary acidic protein (GFAP) in the injury region, and the spinal cord neuronal apoptosis were detected via Western blotting, immunofluorescence labeling and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay, respectively. RESULTS: In group B, there was no significant damage to the structure of spinal cord tissues. In group C, the spinal cord tissues had a disordered structure and significant fragmentation, the damage to grey matter was the greatest. Also, almost all of the grey matter was destroyed and dissolved, with a large number of scars and cavitation, and it was hard to distinguish the gray matter and white matter. In group A, the spinal cord tissues had a clear structure, there were smaller necrotic cavitation regions in the grey-white matter, and the number of cavitation significantly declined compared with that in group C. The results of immunofluorescence assay revealed that the expression of GFAP in spinal cord tissues was the lowest in group B, while it was remarkably decreased in group A compared with that in group C (p<0.05), suggesting that injecting UCMSCs via the caudal vein can prominently reduce the expression of GFAP in spinal cord tissues. Moreover, the spinal cord neuronal apoptosis rate was (4.21±0.19), (0.72±0.21) and (4.57±0.31), respectively, in group A, group B, and group C. It can be seen that the spinal cord neuronal apoptosis rate significantly declined in group A due to the treatment with UCMSCs. Also, the significant difference compared with that in group C, while it was significantly increased in group A compared with that in group B, but lower than group C (p<0.05). According to the results of Western blotting, the protein expression of p-p38 in spinal cord tissues was remarkably decreased in group B compared with that in group A and group C (p<0.05), while it was also markedly decreased in group A compared with that in group C (p<0.05), indicating that injecting UCMSCs via the caudal vein can significantly lower the protein expression of p-p38 in spinal cord tissues. CONCLUSIONS: UCMSCs promote the recovery of neurological function, inhibit the p38 MAPK pathway activated after SCI, and reduce the spinal cord neuronal apoptosis in SCI rats.

[Changes in expression of angiotensin subtype AT1A and AT2 receptors in rats during cardiac remodeling following myocardial infarction].

Immunohistochemical and electron microscopic techniques and image analysis were employed to investigate the regulation of cardiac AT1A and AT2 subtype receptors in rats during cardiac remodeling following myocardial infarction (MI). Positive immunostaining for AT1A and AT2 receptors was observed in myocytes and vessels with AT1A being more than AT2. Three days after MI, disappearance of myocardial cross striation and fibroblast hyperplasia were found with electron microscopy. AT1A receptor protein expression in myocardial noninfarcted portion notably increased compared with that in sham-operated control rats (P < 0.001). No apparent changes were observed in AT2 receptor (P > 0.05). Two weeks after MI, myocyte cross striation and collagen deposition were found. Meanwhile, AT1A receptor staining decreased compared with that of three days after MI (P < 0.01), but there was still more than that of the control (P < 0.05). AT2 receptor was significantly increased compared with that of the sham-operated control rats (P < 0.001). These results suggest that both AT1A and AT2 receptor protein expression was upregulated in noninfarcted myocardium after MI, and the regulation of AT1A and AT2 receptors after MI may be involved in post-infarction cardiac remodeling.

Effect of cathepsin B on thymocyte apoptosis in spontaneously hypertensive rats.

AIM: To further investigate the mechanism of the thymus dysfunction in spontaneously hypertensive rats. METHODS: The location of cathepsin B expression was determined by in situ hybridization. The expression of cathepsin B was analyzed by Northern blot, and thymocyte apoptosis was detected by TUNEL and flow cytometer, respectively. RESULTS: The expression of cathepsin B in thymus paralleled with thymocyte apoptosis both in vitro and in vivo. Cathepsin B transcripts were located in the plasma of thymocytes and were more over-expressed of 6- and 8-week-old SHR than those in the thymus of WKY. CONCLUSION: Thymocyte apoptosis in SHR is increased and this phenomenon is associated with the expression of cathepsin B.