A Cerebellar Tumor-to-Tumor Metastasis in a Patient With Von Hippel-Lindau Disease.

Tumor-to-tumor metastasis in the central nerve system is uncommon in our routine practice. Most reports include metastatic breast cancer into meningioma. Here we report a metastatic clear cell renal cell carcinoma (ccRCC) into a cerebellar hemangioblastoma in a patient with von Hippel-Lindau (VHL) disease. Imaging cannot distinguish metastatic ccRCC from primary cerebellar hemangioblastoma. Immuno-molecular studies are proven to be diagnostic. We also reviewed previously documented tumor-to-tumor metastasis of ccRCC to cerebellar hemangioblastoma in VHL disease. Lastly, we discussed potential mechanisms involved in the metastasis of ccRCC to hemangioblastoma in the cerebellum in patients with VHL.

The risk factors of postoperative hypoxemia in patients with Stanford type A acute aortic dissection.

Hypoxemia is one of the most common complications in patients after Stanford type A acute aortic dissection surgery. The aim of this study was to investigate the association of circulating ANG II level with postoperative hypoxemia and to identify the risk factors for postoperative hypoxemia in Stanford type A acute aortic dissection patients. In this study, 88 patients who underwent Stanford type A acute aortic dissection surgery were enrolled. Postoperative hypoxemia is defined by the oxygenation index (OI). Perioperative clinical data were collected and the serum ANG II and sACE2 levels were measured. The differences in the basic characteristics, intraoperative details, biochemical parameters, laboratory test data and clinical outcomes were compared between the hypoxemia group and the non-hypoxemia group by univariate analysis. Multivariate logistic regression analysis was performed on the variables with P < .1 in univariate analysis or that were considered clinically important to identify risk factors for postoperative hypoxemia. Twenty-five patients (28.4%) were considered to have postoperative hypoxemia (OI ≤ 200 mm Hg). The ANG II concentration remained a risk factor associated with postoperative hypoxemia [OR = 1.018, 95% CI (1.003-1.034), P = .022]. The other risk factors remaining in the logistic regression model were BMI [OR = 1.417, 95% CI (1.159-1.733), P = .001] and cTnI [OR = 1.003, 95% CI (1.000-1.005), P = .032]. Elevated levels of ANG II, BMI and cTnI are risk factors for postoperative hypoxemia in patients with Stanford type A acute aortic dissection.

The anesthetic management of a patient undergoing simultaneous open abdominal aortic aneurysm repair and coronary artery bypass grafting: A case report.

RATIONALE: Surgery for abdominal aortic aneurysm (AAA) and concomitant severe coronary artery disease (CAD) is usually managed in a staged procedure. The anesthesia for concurrent surgery is rare and complex. In this report, we present an unusual case of undergoing simultaneous open abdominal aortic aneurysm (AAA) repair and coronary artery bypass grafting (CABG). PATIENT CONCERNS: A 70-year-old male AAA patient with concurrent triple-vessel CAD underwent a simultaneous surgery. DIAGNOSIS: The patient underwent computed tomography angiography (CTA) and coronary angiography. He was diagnosed with AAA and triple-vessel CAD. INTERVENTIONS: The patient underwent simultaneous surgery. OUTCOMES: The patient underwent anesthesia and surgery smoothly and was discharged on the 13th postoperative day. LESSONS: The anesthetic management of simultaneous open abdominal aortic aneurysm repair and coronary artery bypass grafting is rare and complicated. Reasonable operation and anesthesia protocols, close monitoring and management of hemodynamic changes, and appropriate cell salvage and hemostasis measures are of great significance to increase perioperative safety and reduce the risk of postoperative complications.

Spinal Cord Protection of Aorto-Iliac Bypass in Open Repair of Extent II and III Thoracoabdominal Aortic Aneurysm.

BACKGROUND: Spinal cord injury (SCI) is one of the serious complications of thoracoabdominal aortic aneurysm (TAAA) repair. Cardiopulmonary bypass (CPB) and left heart bypass (LHB) are well-established extracorporeal circulatory assistance methods to increase distal aortic perfusion and prevent spinal cord ischaemia in TAAA repair. Aorto-iliac bypass, a new surgical adjunct offering distal aortic perfusion without the need of complex perfusion skills, was developed as a substitute for CPB and LHB. However, its spinal cord protective effect is unknown. METHODS: The perioperative data of 183 patients who had elective open Crawford extent II and III TAAA repair at our aortic centre from July 2011 to May 2019 were retrospectively analysed. Spinal cord protection was compared between the aorto-iliac bypass group (n=106) and the extracorporeal circulatory assistance group (n=77 [65 CPB, 12 LHB]), and the risk factors for SCI in these patients were explored. RESULTS: Eleven (11) patients had postoperative SCI: five (6.5%) in the extracorporeal circulatory assistance group (four with CPB and one with LHB), and six (5.7%) in the aorto-iliac bypass group. The incidence of SCI was 6.0% (11/183 cases). There was no difference between the aorto-iliac bypass group and the extracorporeal circulatory assistance group (p=1.0), while operation time, proximal aortic clamp time, intercostal artery clamp time, and length of intensive care unit stay were all increased in the latter group. Multivariate logistic regression analysis showed that cerebrospinal fluid pressure (odds ratio [OR] 1.270; 95% confidence interval [CI] 1.092-1.478 [p=0.002]) and lowest haemoglobin on the first postoperative day (OR 0.610; 95% CI 0.416-0.895 [p=0.011]) were the independent predictors of SCI in TAAA repair. CONCLUSIONS: Spinal cord protection of aorto-iliac bypass is comparable to that of CPB and LHB in open TAAA repair.

The Neuroprotective Mechanism of Spinal Cord Stimulation in Spinal Cord Ischemia/Reperfusion Injury.

BACKGROUND: Spinal cord ischemia/reperfusion (I/R) injury following thoracoabdominal aneurysm surgery can lead to severe lower limb neurologic defect. The preliminary result of our study suggested that spinal cord stimulation (SCS) postconditioning effectively protected spinal cord from I/R injury on rabbits. But the mechanism is unknown. In this study, we further investigated the mechanism of SCS postconditioning. METHOD: New Zealand white rabbits were randomly divided into sham, I/R, I/R + 2 Hz SCS, and I/R + 50 Hz SCS group (n = 24/group). Transient spinal cord ischemia was induced by infrarenal aortic balloon occlusion and performed on all rabbits except rabbits of sham group. Rabbits of I/R group received no further intervention. Rabbits of I/R + 2 Hz SCS and I/R + 50 Hz SCS group received 2 Hz or 50 Hz SCS for 30 min at the onset of reperfusion and then daily. The expression of Akt (serine-threonine kinase)/p-Akt, STAT3 (signal transducer and activator of transcription 3)/p-STAT3 and GSK-3ß (glycogen synthase kinase)/p-GSK-3ß of spinal cord were measured by Western blot analysis at 8 h, 1 day, 3 day, and 7 day of reperfusion. RESULT: The Akt expressions of sham, I/R, I/R + 2 Hz SCS, and I/R + 50 Hz SCS group were not significantly different at all prescribed time points, while the p-Akt expression of I/R + 2 Hz SCS group was significantly higher than that of I/R group and sham group at all prescribed time points; The STAT3 and p-STAT3 expression of I/R, I/R + 2 Hz SCS, and I/R + 50 Hz SCS group were not significantly different at all prescribed time points except that at 1day of reperfusion the p-STAT3 expression of I/R + 50 Hz SCS group was significantly lower than I/R group. The GSK-3ß and p-GSK-3ß expressions of I/R, I/R + 2 Hz SCS and I/R + 50 Hz SCS group were not significantly different at all prescribed time points. CONCLUSION: The neuroprotective effect of 2 Hz SCS postconditioning in spinal cord I/R injury is related to Akt activation but not regulation of STAT3 and GSK-3ß phosphorylation.

Factors Influencing the Steady-State Plasma Concentration of Imatinib Mesylate in Patients With Gastrointestinal Stromal Tumors and Chronic Myeloid Leukemia.

Imatinib mesylate (IM) is the standard treatment for advanced, metastatic gastrointestinal stromal tumors (GISTs) and chronic myeloid leukemia (CML) with a fixed daily standard dosage via the oral route. Interindividual and intraindividual variability in plasma concentrations have been closely linked to the efficacy of IM therapy. Therefore, this review identifies and describes the key factors influencing the plasma concentration of IM in patients with GISTs and CML. We used the following keywords to search the PubMed, EMBASE, Ovid, Wangfang, and CNKI databases to identify published reports: IM, plasma concentration, GISTs, CML, drug combination/interaction, pathology, and genotype/genetic polymorphism, either alone or in combination. This literature review revealed that only 10 countries have reported the mean concentrations of IM in GISTs or CML patients and the clinical outcomes in different ethnic groups and populations. There were totally 24 different gene polymorphisms, which were examined for any potential influence on the steady-state plasma concentration of IM. As a result, some genotype locus made discrepant conclusion. Herein, the more sample capacity, multicenter, long-term study was worthy to carry out. Eleven reports were enumerated on clinical drug interactions with IM, while there is not sufficient information on the pharmacokinetic parameters altered by drug combinations with IM that could help in investigating the actual drug interactions. The drug interaction with IM should be paid more attention in the future research.

Complete Depletion of Daratumumab Interference in Serum Samples from Plasma Cell Myeloma Patients Improves the Detection of Endogenous M-Proteins in a Preliminary Study.

BACKGROUND: Therapeutic humanized IgG1 kappa monoclonal antibody (t-mAb), daratumumab (DARA) is a Food and Drug Administration approved drug for the treatment of relapsed/refractory plasma cell myeloma (PCM). DARA appears on serum protein electrophoresis (SPEP) and on serum immunofixation (sIFE) as an IgG kappa monoclonal immunoglobulin protein (M-protein), complicating the assessment of the patients' response to therapy. A more ominous threat to patient safety can occur with the misinterpretation of the presence of a small t-mAb spike as being the residual product of the patient's neoplastic clone, presented either as oligoclonality or new clonality, which could result in incorrect interpretation of failure to achieve remission. METHODS: In this report, we describe a novel and cost-effective technique based on biotinylated recombinant CD38 and streptavidin-coated magnetic beads to capture and remove residual DARA present in PCM patient serum samples. The treated samples are then run like regular samples on SPEP and sIFE. We validated this simple technique in DARA-spiked PCM samples and patient samples on DARA treatment. RESULTS: Our simple capture technique completely extracted DARA in all of the tested serum specimens and allowed the assessment of residual M-protein without DARA interference. The results were reproducible and highly specific for DARA, and did not have any impact on endogenous M-protein migration and quantification by SPEP and sIFE. The cost of this technique is much lower and it can be performed in-house with a very short turnaround time compared to the currently available alternative methods. There is a great need for such reflex technologies to avoid interpretation errors. CONCLUSIONS: This method is an effective way to eliminate DARA interference in SPEP and sIFE, and can be easily implemented in any clinical laboratory without any patent restriction. This simple technique can be adopted for other t-mAbs using their respective ligands and will help to reduce additional doses of toxic treatment and further testing in patients on t-mAbs with a false positive M-protein spike.

Neuroprotective mechanism involved in spinal cord stimulation postconditioning.

OBJECTIVES: Delayed paraplegia developed postoperatively after thoracoabdominal aneurysm surgery is primarily associated with spinal cord ischemia/reperfusion injury. Our previous study suggested that spinal cord stimulation postconditioning protected the spinal cord from ischemia/reperfusion injury through microglia inhibition. In this study, we further investigated whether α7 nicotinic acetylcholine receptors were involved in the neuroprotective mechanism of spinal cord stimulation. METHODS: Rabbits were randomly assigned to sham, control, 2 Hz, α-bungarotoxin, and 2 Hz-α-bungarotoxin groups (n = 24/group). Transient spinal cord ischemia was performed on all rabbits except rabbits in the sham group. Rabbits in the control group received no further intervention, rabbits in the 2 Hz group were given 2 Hz spinal cord stimulation, rabbits in the α-bungarotoxin group received prescribed intrathecal α-bungarotoxin (α-bungarotoxin, a specific α7 nicotinic acetylcholine receptor antagonist) injections, and rabbits in the 2 Hz-α-bungarotoxin group received both α-bungarotoxin injections and 2 Hz spinal cord stimulation. Hind-limb neurologic function was assessed, and spinal cord histologic examination, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining, and microglia staining were performed at 8 hours, 1 day, 3 days, and 7 days of reperfusion. RESULTS: Rabbits in the 2 Hz group had significantly better neurologic functions, more α-motor neurons, and lower terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling-positive neuron rates and microglia area/anterior horn area ratios (microglia area ratios) than the control group. The neurologic functions of the α-bungarotoxin group were significantly worse than those of the control group, whereas other results were not significantly different from the control group. The results of the 2 Hz-α-bungarotoxin group were insignificant to the control group except for the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling-positive neuron rates, which were significantly lower than in the control group. CONCLUSIONS: The neuroprotective effects of spinal cord stimulation postconditioning against spinal cord ischemia/reperfusion injury were partially mediated by activating α7 nicotinic acetylcholine receptors.

Spinal cord stimulation postconditioning reduces microglial activation through down-regulation of ERK1/2 phosphorylation during spinal cord ischemic reperfusion in rabbits.

Microglial activation plays a critical role in spinal cord ischemic reperfusion injury. Spinal cord stimulation preconditioning and postconditioning has shown spinal cord protection in ischemic reperfusion injury in animal studies. However, whether spinal cord stimulation could reduce microglial activation is still unclear. In this study, rabbits experienced 28-min infrarenal aorta occlusion and reperfusion for 8 h, 1, 3, and 7 days correspondingly. Immediately after reperfusion, rabbits received spinal cord stimulation of 2 or 50 Hz for 30 min and daily for a week. The results showed that spinal cord stimulation of 2 Hz reduced microglial activation. Microglial activation was accompanied with up-regulated p-ERK1/2, and microglial inhibition by 2 Hz spinal cord stimulation was associated with down-regulated p-ERK1/2. Spinal cord stimulation increased the expression of IL-1ß. Our results revealed, for the first time, that spinal cord stimulation postconditioning suppresses microglial activation during spinal cord ischemic reperfusion by down-regulation of p-ERK1/2, which may be the protective mechanism of spinal cord stimulation.

The Protective Effect of Spinal Cord Stimulation Postconditioning Against Spinal Cord Ischemia/Reperfusion Injury in Rabbits.

BACKGROUND: Delayed paraplegia due to spinal cord ischemia/reperfusion injury (IRI) remains one of the most severe complications of thoracoabdominal aneurysm surgery, for which effective prevention and treatment is still lacking. OBJECTIVES: The current study investigates whether spinal cord stimulation (SCS) postconditioning has neuroprotective effects against spinal cord IRI. METHOD: Ninety-six New Zealand white male rabbits were randomly divided into four groups as follows: a sham group and three experimental groups (C group, 2 Hz group, and 50 Hz group) n = 24/group. Spinal cord ischemia was induced by transient infrarenal aortic balloon occlusion for 28 min, after which rabbits in group C underwent no additional intervention, while rabbits in the other two experimental groups underwent 2 Hz or 50 Hz epidural SCS for 30 min at the onset of reperfusion and then daily until sacrifice. Hind limb neurologic function of rabbits was assessed using Jacob scale. Lumbar spinal cords were harvested immediately after sacrifice for histological examination and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining. The number of viable α-motor neurons in ventral horn was counted and TUNEL-positive rate of α-motor neurons was calculated. RESULT: Spinal cord IRI was caused by transient infrarenal aorta occlusion for 28 min. Both 2 Hz and 50 Hz SCS postconditioning had neuroprotective effects, particularly the 2 Hz SCS postconditioning. Comparing to C group and 50 Hz group, rabbits in the 2 Hz group demonstrated better hind limb motor function and a lower rate of TUNEL-positive α-motor neuron after eight hours, one day, three days, and seven days of spinal cord reperfusion. More viable α-motor neurons were preserved after one and three days of spinal cord reperfusion in 2 Hz group rabbits than in C group and 50 Hz group rabbits. CONCLUSION: SCS postconditioning at 2 Hz protected the spinal cord from IRI.

IL-17A Inhibits Osteogenic Differentiation of Bone Mesenchymal Stem Cells via Wnt Signaling Pathway.

BACKGROUND Interleukin-17A (IL-17A) is not only an important modulator of inflammatory reactions, but also affects bone metabolism, which is involved in osteogenic differentiation of stem cells. However, the role and mechanism of IL-17A in osteogenic differentiation of bone mesenchymal stem cells (BMSCs) are not fully understood. In this study, we investigated the role and mechanism of IL-17A in osteogenic differentiation of BMSCs. MATERIAL AND METHODS The osteogenic differentiation of BMSCs was induced by osteoblast-induction medium with IL-17A or without IL-17A. The osteogenic differentiation of BMSCs was confirmed by the alkaline phosphatase and alizarin red staining. The lentiviral plasmid was used to construct the sFRP1-shRNA expression vector. The associated osteogenic differentiation marks (RUNX2, ALP, OPN), Wnt signaling pathway inhibitor (sFRP1), and modulators of Wnt signaling pathway (Wnt3, Wnt6) were detected by qRT-PCR and Western blot method. RESULTS The results showed that the addition of IL-17A inhibited osteogenic differentiation of BMSCs. IL-17A induced up-regulated expression of sFRP1 and down-regulated expression of Wnt3 and Wnt6 in BMSCs. In addition, sFRP1-shRNA abolished the inhibition effect of IL-17A in osteogenic differentiation of BMSCs and induced up-regulated expression of Wnt3 and Wnt6 in the Wnt signaling pathway in BMSCs. CONCLUSIONS Our findings show that IL-17A inhibits osteogenic differentiation of bone mesenchymal stem cells via the Wnt signaling pathway.

Mechanism and early intervention research on ALI during emergence surgery of Stanford type-A AAD: Study protocol for a prospective, double-blind, clinical trial.

BACKGROUND: Stanford type-A acute aortic dissection (AAD) is a severe cardiovascular disease demonstrating the characteristics of acute onset and rapid development, with high morbidity and mortality. The available evidence shows that preoperative acute lung injury (ALI) induced by Stanford type-A AAD is a frequent and important cause for a number of untoward consequences. However, there is no study assessing the incidence of preoperative ALI and its independent determinants before Standford type-A AAD surgery in Chinese adult patients. METHODS/DESIGN: This is a prospective, double-blind, signal-center clinical trial. We will recruit 130 adult patients undergoing Stanford type-A AAD surgery. The incidence of preoperative ALI will be evaluated. Perioperative clinical baselines and serum variables including coagulation, fibrinolysis, inflammatory, reactive oxygen species, and endothelial cell function will be assayed. The independent factors affecting the occurrence of preoperative ALI will be identified by multiple logistic regression analysis. TRIAL REGISTRATION: ClinicalTrials.gov (https://register.clinicaltrials.gov/), Registration number NCT01894334.

Xenon-delayed postconditioning attenuates spinal cord ischemia/reperfusion injury through activation AKT and ERK signaling pathways in rats.

Previous studies have shown that xenon-delayed postconditioning for up to 2h after reperfusion provides protection against spinal cord ischemia/reperfusion (I/R) injury in rats. This study was designed to determine the roles of phosphatidylinositol 3-kinase (PI3K)-Akt and extracellular signal-regulated kinase (ERK) in this neuroprotection. The rats were randomly assigned to the following nine groups (n=16∗9): 1) I/R+N2 group, 2) I/R+Xe group, 3) I/R+PD98059+N2 group (ERK blocking agent), 4) I/R+wortmannin+N2 group (PI3K-Akt blocking agent), 5) I/R+PD98059+Xe group, 6) I/R+wortmannin+Xe group, 7) I/R+DMSO+Xe group (dimethyl sulfoxide, vehicle control), 8) I/R+DMSO+N2 group, and 9) sham group (no spinal cord ischemia and no xenon). Spinal cord ischemia was induced for 25min in male Sprague-Dawley rats. Neurological function was assessed using the Basso, Beattie, and Bresnahan (BBB) open-field locomotor scale at 6, 12, 24 and 48h after reperfusion. Histological examination of the lumbar spinal cord was performed using Nissl staining and TUNEL staining at 4 (n=8) and 48 (n=8)h after reperfusion. Western blotting was performed to evaluate p-Akt and p-ERK expression in the spinal cord at 4 (n=8) and 48 (n=8) h after reperfusion. Compared with the sham group, all rats in the I/R groups had lower BBB scores, fewer normal motor neurons, more apoptotic neurons and lower p-Akt and p-ERK levels at each time point (P<0.05). Compared with the I/R group, rats in the I/R+Xe group had higher neurological scores, more normal motor neurons, fewer apoptotic neurons and significantly higher levels of p-Akt and p-ERK at each time point (P<0.05). Compared with the I/R+Xe group, the I/R+PD98059+Xe and I/R+wortmannin+Xe groups showed worse neurological outcomes and less p-Akt and p-ERK at each time point (P<0.05). These results suggest that xenon-delayed postconditioning improves neurological outcomes to spinal cord I/R injury in rats through the activation of the AKT and ERK signaling pathways.

An atypical presentation of chronic Stanford type A aortic dissection during pregnancy.

Aortic dissection is a rare but devastating disease during pregnancy, usually presenting with sharp pains on the chest or back. We report a pregnant woman suffering from chronic Stanford type A aortic dissection presented with atypical symptoms without pain in the third trimester with markedly dilated aortic root and congestive heart failure, who received concomitant cesarean delivery and aortic repair with good maternal and fetal outcomes. Multidisciplinary approach and tight hemodynamic control are very important. More attention should be paid to those atypical symptoms so as to early identify this scarce but disastrous disease during pregnancy.

Aorta-Iliac Bypass in Thoracoabdominal Aortic Aneurysm Repair in Young Chinese Patients.

BACKGROUND: Many surgical methods of thoracoabdominal aortic aneurysm repair (TAAAR) have been introduced over the past several decades, with varying degrees of success. We developed an aorta-iliac bypass technique to treat thoracoabdominal aortic aneurysm (TAAA) in young Chinese patients. The aim of this study is to evaluate the results of this technique intraoperatively and postoperatively. METHODS: From June 2014 to March 2015, 28 patients underwent TAAAR using aorta-iliac bypass technique. A four-branched tetrafurcate graft was used. Two branches of the graft are sutured to bilateral common iliac arteries in an end-to-side fashion. The trunk of the graft was sutured to the proximal descending aorta in an end-to-end fashion. Then aorta-iliac bypass was established, and the lower extremities, viscera organ and spinal cord (SC) obtained perfusion from proximal descending aorta via the bypass graft. The thoracic and abdominal aorta were clamped in a staged fashion. The patent segmental arteries (SAs), and visceral arteries (coeliac trunk, superior mesenteric arteries, and renal arteries) were reattached sequentially. Evoked potential (EP) monitoring was adopted to assess the SC ischaemia throughout the procedure. The postoperative outcomes and follow-up results of this technique were evaluated. RESULTS: There was no in-hospital mortality. Complications included acute kidney dysfunction and pulmonary haemorrhage in one case (3.6%) each. The SAs were reattached in all cases. The EP wave disappeared after proximal descending aorta was clamped, and gradually recovered after the patent SAs reattached. The median follow-up after operation was eight months (range, 1-10 months). There was no delayed neurologic deficit or late death. CONCLUSIONS: Thoracoabdominal aortic aneurysm repair using aorta-iliac bypass may be a simple and safe choice for young Chinese patients with thoracoabdominal aortic aneurysms.

Serine-threonine protein kinase activation may be an effective target for reducing neuronal apoptosis after spinal cord injury.

The signaling mechanisms underlying ischemia-induced nerve cell apoptosis are poorly understood. We investigated the effects of apoptosis-related signal transduction pathways following ischemic spinal cord injury, including extracellular signal-regulated kinase (ERK), serine-threonine protein kinase (Akt) and c-Jun N-terminal kinase (JNK) signaling pathways. We established a rat model of acute spinal cord injury by inserting a catheter balloon in the left subclavian artery for 25 minutes. Rat models exhibited notable hindlimb dysfunction. Apoptotic cells were abundant in the anterior horn and central canal of the spinal cord. The number of apoptotic neurons was highest 48 hours post injury. The expression of phosphorylated Akt (p-Akt) and phosphorylated ERK (p-ERK) increased immediately after reperfusion, peaked at 4 hours (p-Akt) or 2 hours (p-ERK), decreased at 12 hours, and then increased at 24 hours. Phosphorylated JNK expression reduced after reperfusion, increased at 12 hours to near normal levels, and then showed a downward trend at 24 hours. Pearson linear correlation analysis also demonstrated that the number of apoptotic cells negatively correlated with p-Akt expression. These findings suggest that activation of Akt may be a key contributing factor in the delay of neuronal apoptosis after spinal cord ischemia, particularly at the stage of reperfusion, and thus may be a target for neuronal protection and reduction of neuronal apoptosis after spinal cord injury.

Preoperative transcatheter occlusion of bronchopulmonary collateral artery reduces reperfusion pulmonary edema and improves early hemodynamic function after pulmonary thromboendarterectomy.

OBJECTIVE: The present study assessed the effectiveness of preoperative transcatheter occlusion of the bronchopulmonary collateral artery (PTOBPCA) in reducing reperfusion pulmonary edema after pulmonary thromboendarterectomy (PEA). METHODS: The data from 155 patients with chronic thromboembolic pulmonary hypertension at Anzhen Hospital, treated from January 2007 to August 2013, with PEA were retrospectively reviewed. The patients were classified into a control (group A, n = 87) and treated (group B, underwent PTOBPCA, n = 68) group. The reperfusion pulmonary edema incidence, mechanical ventilation and intensive care unit hospitalization duration, and hemodynamic function were compared between the 2 groups. RESULTS: Of the 87 patients in group A, 5 died in-hospital (5.7% mortality); no patient in group B died (0% mortality; P = .035). In group A, 9 patients (10.3%) required extracorporeal membrane oxygenation (ECMO) after PEA; 1 patient (1.5%) in group B required ECMO (chi-square test, P = .026, χ(2) = 4.980). Group B had shorter intubation and intensive care unit hospitalization times, lower mean pulmonary artery pressures and pulmonary vascular resistance, higher partial pressures of oxygen in arterial blood and oxygen saturation, and decreased medical expenditure compared with group A. During a mean 37.1 ± 21.4 months of follow-up, 3 patients in group A and 2 in group B died; however, the difference in the actuarial survival at 3 years postoperatively between the 2 groups was not statistically significant. CONCLUSIONS: PTOBPCA can reduce the incidence of reperfusion pulmonary edema, shorten intensive care unit hospitalization and intubation duration, improve early hemodynamic function, and reduce ECMO usage after PEA.

Pulmonary oligemia maneuver can alleviate pulmonary artery injury during pulmonary thromboendarterectomy procedure.

BACKGROUND: Pulmonary thromboendarterectomy (PTE) has evolved as a treatment of choice for chronic thromboembolic pulmonary hypertension (CTEPH). This study aimed to characterize if pulmonary oligemia maneuver (POM) can alleviate pulmonary artery injury during PTE procedure. METHODS: A total of 112 cases of CTEPH admitted to Beijing Anzhen Hospital from March 2002 to August 2011 received PTE procedure. They were retrospectively classified as non-POM group (group A, n = 55) or POM group (group B, n = 57). Members from group B received POM during rewarming period, whereas members from group A did not. RESULTS: There were three (5.45%) early deaths in group A, no death in group B (0) (Fisher's exact test, P = 0.118). Six patients in group A needed extracorporeal membrane oxygenation (ECMO) as life support after the PTE procedure, no patients in group B needed ECMO (Fisher's exact test, P = 0.013). The patients in group B had a shorter intubation and ICU stay, lower mean pulmonary arterial pressure (mPAP) and pulmonary vascular resistance (PVR), higher partial pressure of oxygen in artery (PaO2) and arterial oxygen saturation (SaO2) and less medical expenditure than patients in group A. With a mean follow-up time of (58.3 ± 30.6) months, two patients in group A and one patient in group B died. The difference of the actuarial survival after the procedure between the two groups did not reach statistical significance. Three months post the PTE procedure, the difference of residual occluded pulmonary segment between the two groups did not reach statistical significance (P = 0.393). CONCLUSION: POM can alleviate pulmonary artery injury, shorten ICU stay and intubation time, and lower down the rate of ECMO after PTE procedure.

[Analysis of risk factors of postoperative hemodialysis in patients undergoing off-pump coronary artery bypass grafting].

OBJECTIVE: To investigate the risk factors of postoperative hemodialysis in patients undergoing off-pump coronary artery bypass grafting (OPCAB). METHODS: The perioperative data of 2379 consecutive patients undergoing OPCAB from November 2007 to February 2009 were analyzed retrospectively. Patients were divided into dialysis group and non-dialysis group according to their use of hemodialysis therapy or not. RESULTS: Fifty-four patients experienced hemodialysis postoperatively. The incidence of hemodialysis was 2.3%, the mortality rate of dialysis group and non-dialysis group was 18.5% and 0.9% respectively. Univariate analysis showed that these factors significantly related with the postoperative dialysis:intraoperative ventricular fibrillation, emergent cardiopulmonary bypass, preoperative atrial fibrillation, intraoperative atrial fibrillation, preoperative renal dysfunction, intraoperative high-dose adrenaline usage, ventricular aneurysm, combined valvular disease, hypertension, age and numbers of grafting vessels. Multivariate logistic regression showed that intraoperative ventricular fibrillation, intraoperative high-dose adrenaline usage, hypertension, age and the numbers of grafting vessel were the risk factors of postoperative hemodialysis for patients undergoing OPCAB surgery. CONCLUSION: Intraoperative ventricular fibrillation, intraoperative high-dose adrenaline usage, hypertension, age and the numbers of grafting vessels were the independent predictors of postoperative hemodialysis in patients undergoing OPCAB surgery.

[Studies on the alkaloids from roots of Corydalis impatiens].

OBJECTIVE: To study the alkaloids from Corydalis impatiens. METHODS: The alkaloids were isolated and purified by chromatography and their structures were identified by spectral data and others methods. RESULTS: Seven alkaloids were isolated and identified as bicuculline(1), ochotensine(2), ochotensimine(3), ochrobirine(4), tetrahydrothalifendine(5), norochotensimine(6), N-methylactinodaphnine(7). CONCLUSION: All these compounds are isolated from this plant for the first time.