Hemoadsorption and Coagulation Systemic Rebalance in Patients Undergoing Nonelective Cardiac Surgery and Treated with Antithrombotics.

INTRODUCTION: Insufficient withdrawal duration of antithrombotics leads to excessive bleeding after major surgery. We hypothesize that intraoperative hemoadsorption (HA) can reduce postoperative allogeneic transfusion requirements and excessive bleeding events (EBE), without an increase in ischemic/thromboembolic events (ITE) in patients who have taken antithrombotics and undergone nonelective cardiac surgery. METHODS: A total of 460 patients admitted to our hospital from 2018 to 2022 were included in this study and divided into two groups: HA and non-HA. Because of the risk of bias due to differences in antithrombotic type, withdrawal duration, or basic coagulation function, propensity score matching was used for analyses. RESULTS: Out of 154 cases in the HA group, 144 pairs were successfully matched. No HA safety events such as hemolysis, hypotension, or device failure occurred. After matching, the two groups were found to be comparable in preoperative antithrombotic type, withdrawal duration, platelets and coagulation function, and demographic and perioperative characteristics. Although the HA group did not have a reduced incidence of EBE, this group exhibited significant decreases in the transfusion rate and volume, the incidence of ITE, acute kidney injury, and central nervous system injury. CONCLUSIONS: For patients who have undergone nonelective cardiac surgery and taken antithrombotics, HA can simply and safely rebalance the postoperative coagulation system and have associations with reduced transfusion and postoperative ITE.

[Galectin3 Regulates Transforming Growth Factor-ß-induced Epithelial-mesenchymal].

Objective To explore the role of Galectin3 in transforming growth factor-ß(TGF-ß)-induced epithelial-mesenchymal transition (EMT) in A549 cells. Methods Galectin3 was over-expressed in an A549 cell line. EMT was induced in lung cancer A549 cells by adding TGF-ß. The expressions of Galectin3,E-cadherin,and vimentin were determined by Western blot. The protein expression of E-cadherin and the morphological changes of the cells were detected by immunofluorescence. Cellular proliferation was analyzed with cell counting kit-8,and the cellular migration and invasion was measured by scratches healing and Transwell assay,respectively.Results When only Galectin3 was over-expressed in A549 cell line,the expression levels of EMT-related proteins such as E-cadherin and vimentin were not changed,and the abilities of cellular proliferation,invasion,and migration were not changed either. When the EMT was induced by TGF-ß in A549 cells,the E-cadherin expression was down-regulated and the vimentin expression was up-regulated in A549 cells with Galectin3 over-expression. There was no significant change in cellular proliferation,whereas the abilities of cellular invasion and migration were enhanced.Conclusion The TGF-ß-induced EMT in A549 cells can be enhanced by Galectin3.

Chest wall tumors: Diagnosis, treatment and reconstruction.

The aim of the present study was to determine a suitable procedure for the treatment of chest wall neoplasms with less potential risk and an increased rate of survival. Fifty patients with suspected chest wall malignancies were analyzed using various preliminary investigation tools. Whole-chest scanning was performed in all the patients. The patients were subsequently subjected to biopsies for further confirmation of the neoplasm. All such patients were then treated with a surgical approach and radiation therapy, with a follow-up period lasting up to six years. The majority of the patients showed improved survival rates relative to conventional therapies. The survival rates of patients suffering from osteosarcoma (78%) were higher those of patients with rhabdomyosarcoma (73%) and malignant small round cell tumors (64%). The survival and the mortality rates of the patients with synovial sarcoma and fibrosarcoma were the same. This study, which was conducted on a small group of patients, has provided guidance for further studies on tumors of the chest wall, which may, in turn, increase the longevity of affected patients.

Kank1 reexpression induced by 5-Aza-2'-deoxycytidine suppresses nasopharyngeal carcinoma cell proliferation and promotes apoptosis.

Kank1, which was first described as a potential tumor suppressor for renal cell carcinoma (RCC), mapped to 9p24.3 and encoded an ankyrin-repeat domain-containing protein. Its frequent deletion was found to be associated with several human malignant tumors, cerebral palsy, and neuronal and developmental diseases. However, its functional role in nasopharyngeal cancer (NPC) was still unknown. In the present study, we found that Kank1 expression was down-regulated in NPC cells than in human nasopharyngeal epithelial cell line NP69 and demethylating agent 5-aza-2'-deoxycytidine (5-aza-CdR) could improve its mRNA and protein expression level. Further studies demonstrated that DNA methylation might be the mainly cause for Kank1 decreased expression and restored Kank1 expression mediated by 5-aza-CdR played a key role in suppressing NPC cells growth and inducing its apoptosis. Our primary results revealed new function of Kank1 for NPC and implied that epigenetic regulation especially demethylation may have a potential value for NPC treatment.

Association of BTBD7 with Metastasis and Poor Prognosis in Non-Small-Cell Lung Cancer Patients.

Metastasis in lung cancer portends a poor prognosis, and the epithelial-mesenchymal transition (EMT) in lung cancer cells is considered a prerequisite to achieve metastatic potential. Recent studies indicate that BTB/POZ domain-containing protein 7 (BTBD7) regulates EMT-associated proteins in human malignancies and however, the role of BTBD7 in lung cancer have not been identified. In present study, we examined BTBD7 expression status and its association with unfavorable clinical features in non-small-cell lung cancer (NSCLC). Firstly, we studied the fresh specimens, and found that both mRNA and protein expression levels of BTBD7 in NSCLC tissue were significantly increased compared with the adjacent nontumorous lung tissue. Then, we determined BTBD7 protein expressions in the paraffin-embedded samples from NSCLC patients, and analyzed the relations of BTBD7 expression with clinicopathologic features of the patients. The results showed that incidence of metastasis in patients with positive BTBD7 expression was significantly higher than that in those with negative BTBD7 expression, and the positive BTBD7 expression rate in metastatic cases was significantly higher than that in non-metastatic ones; furthermore, Cox regression analyses revealed that BTBD7 was an independent risk factor for either metastasis or survival in NSCLC patients. Thus, we conclude that BTBD7 contributes to metastasis of NSCLC and BTBD7-positive NSCLC may have a high potential for metastasis and thereby a poor prognosis.

Ischemic postconditioning reduces ischemic reperfusion injury of non-heart-beating donor grafts in a rat lung transplant.

OBJECTIVES: This study was designed to see if ischemic postconditioning could attenuate ischemic reperfusion injury of transplanted lungs recovered from non-heart-beating donors. MATERIALS AND METHODS: Forty Sprague-Dawley rats were randomized into 2 groups: the control group and the ischemic postconditioning group, with 10 donor rats paired with 10 recipient rats in each group. Twenty rats underwent a left lung transplant from non-heart-beating donors with a warm ischemia time of 36.7 ± 5.62 minutes. In the ischemic postconditioning group, 5 cycles of 1-minute reperfusion and 1-minute reocclusion at the onset of reperfusion were applied as postconditioning. Arterial blood gas, wet-to-dry lung weight ratio, activities of malondialdehyde and superoxide dismutase, and expressions of apoptosis and ICAM-1 mRNA were compared. RESULTS: When compared with the control group 4 hours after reperfusion, PaO2 was higher, and wet-to-dry lung weight ratio was lower, in the ischemic postconditioning group, and expression of apoptosis and ICAM-1 mRNA as well as activity of malondialdehyde were lower, while superoxide dismutase activity was higher in the ischemic postconditioning group. CONCLUSIONS: Ischemic postconditioning can reduce ischemic reperfusion injury of lungs recovered from non-heart-beating donors and preserve lung function by reducing reactive oxygen species and inhibiting apoptosis and inflammation.

[Cardiopulmonary protection of ischemic postconditioning in cardiac surgery in children with tetralogy of Fallot].

OBJECTIVE: Ischemic postconditioning effectively minimizes the ischemic/reperfusion injury, and the large series of case reports on its protective effects in cardiac surgery are limited. A randomized trial was conducted to investigate the effect of ischemic postconditioning on cardiopulmonary protection in children undergoing cardiac surgery for tetralogy of Fallot. METHODS: One hundred and five-children with tetralogy of Fallot undergoing surgery were randomly assigned to control (n=58) and ischemic postconditioning groups (n=47). Ischemic postconditioning was performed by intermittent aortic clamping after reperfusion. After surgery, the duration of intensive care unit (ICU) stay, capacity of blood transfusion, hemodynamics, inotropic scores, respiratory function, and release of blood lactate were assayed. RESULTS: There was a significant decrease in the ICU stay in the postconditioned group compared with the control group (37+/-21 hrs vs 54+/-26 hrs; P<0.05 ). The capacity of blood transfusion (308+/-230 mL vs 526+/-515 mL; P<0.05) and the inotropic scores (5.9+/-5.0 vs 10.3+/-7.7; P<0.05) in the postconditioned group were significantly reduced compared with those in the control group. Blood lactate contents in the postconditioned group was significantly lower that those in the control group 1, 3, 6, 9, 12 and 20 hrs after surgery. The postconditioned group showed more improved hemodynamics and respiratory function than the control group. CONCLUSIONS: Ischemic postconditioning may provide clinical benefits with respects to myocardial and pulmonary protections in children undergoing repair for tetralogy of Fallot.

[Effect of HOE642 on cardiac myocyte apoptosis in rat non heart-beating donors].

OBJECTIVES: To investigate the effect of HOE642 on cardiac myocyte apoptosis of the heterotopic heart transplantation of rat non heart-beating donors. METHODS: Totally 112 male Sprague-Dawley rats were randomly divided into 7 groups (n=16 in each group) C, the control group (normal hearts); S10, S30, and S45 (groups of transplanted hearts after 10, 30, and 45 minutes of asystole); and SH10, SH30, and SH45 (groups of transplanted hearts after 10, 30, and 45 minutes of asystole and infused with HOE642). After rata in the experimental groups were killed by warm ischemia the donators of the S10, S30 and S45 groups were infused with 5TH-1 for 30 minutes, and the dead rats in group SH10, SH30, and SH4 were infused with STH-1 and HOE642 (20 micromol/L) for 30 minutes. Heterotopic heart transplantation were processed by the method of neck Cuff. The heart specimens of S10, SH10, S30, and SH30 groups were taken after 48 hours of transplantation, and the heart specimens of S45 and SH45 groups were taken immediately after transplantation. Then apoptotic myocytes were detected with terminal deoxynucleotide transferase-mediated deoxyuridine-biotin nick end labeling method and the expressions of Bcl-2, Bax, and Caspase-3 proteins were detected by immunohistochemistry. RESULTS: The rats were discerned death when cardiac electric wave vanished after 9-11 minutes of bloodletting by transsection of abdominal aorta. The number of positive cardiac muscle cells in S10 and S30 groups were significantly larger than those in group SH10 and SH30 (P < 0.05). The levels of Bcl-2 protein expression in S10 and S30 groups were significantly lower than those in SH10 and SH30 groups (P < 0.05). The levels of Bax and Caspase-3 protein expression were significantly higher than those in SH10 and SH30 groups (P < 0.05). CONCLUSIONS: The rat model of a heterotopic heart transplantation on the cervical part is a convenient animal model for cardiac muscle protection. HOE642 can suppress rat cardiac muscle cells apoptosis (within 30 min) after death caused by warm ischemia.

[Effect of cariporide on the expression of bcl-2 and bax genes after neck heart transplantation from non heart-beating rats caused by warm ischemia].

OBJECTIVE: To detect the expression of bcl-2 and bax genes after heterotopic heart transplantation in rats that died of warm ischemia, and to explore the effect of cariporide on the protection of the ratos non heart-beating donors. METHODS: One hundred and twelve clearing Sprague-Dawley male rats were divided into 7 groups at random (each group contained 16 rats): the control group (Group C), the groups of transplanted hearts after 10, 30, and 45 min of asystolia (Group S10,S30,and S45), and the groups of transplanted hearts after 10,30, and 45 min of asystolia and infused with cariporide(Group SH10,SH30, and SH45).The experimental groups were sacrificed totally by warm ischemia, and heterotopic heart transplantation was processed by the Cuff method. The heart samples of S10,SH10,S30, and SH30 groups were taken at 48 hours after the transplantation, and the heart samples of S45, and SH45 groups were taken just after transplantation. The expression of bcl-2 and bax genes were detected by RT-PCR. RESULTS: The death of rats was affirmed when cardiac electric waves vanished after 9~11 minutes of transsection of abdominal aorta. On the RT-PCR test, the expression of bcl-2 gene was the highest and ROD value was maximum in the control group. The expression of bax gene was the lowest and ROD value was minimum in the control group. The ROD value of bcl-2 genes in S10 and S30 groups was less than that in SH10 and SH30 group. The ROD value was just the opposite, and there was stastistical difference (P<0.05).There was no statistical difference between Group S45 and Group SH45 (P>0.05). CONCLUSION: The model of heteroto-pic neck heart transplantation is a convenient animal model for the cardiac muscle protection. Cariporide can suppress the apoptosis of cardiac muscle cells in rats (within 30 min) after death caused by warm ischemia.