Myelopreservation with Trilaciclib in recurrent advanced ovarian cancer: a case report.

Ovarian cancer is a prevalent malignant tumor of the female reproductive system, often remaining concealed until it reaches an advanced stage. The standard treatment protocol includes cytoreductive surgery for ovarian cancer plus postoperative consolidation chemotherapy and maintenance therapy, although it carries a high recurrence rate. During the treatment period, chemotherapy can lead to bone marrow suppression, a condition known as Chemotherapy-Induced Myelosuppression (CIM). This suppression may necessitate dose reduction or chemotherapy treatment cycle delay. In severe cases, CIM can result in infection, fever, and potential harm to the patient's life. Here, we report a case of a female patient with ovarian malignant tumor of biochemical recurrence who treated with chemotherapy combined with Trilaciclib, following previous perioperative chemotherapy with occurrence of severe CIM. It involves an intravenous injection of Trilaciclib before chemotherapy, which significantly abates the side effects of chemotherapy, reduces the occurrence of severe CIM, improves the patients' quality of life, and decreases the economic burden of hospitalization. We hope that this retrospective analysis of the case may serve as a reference in preventing and treating severe CIM during chemotherapy in some patients with malignant tumors, ultimately benefiting more patients with tumors.

Feasibility and safety of Post-Urgent PCI Same-DaY discharge (PUSDY Trial) in China: protocol for a multicentre randomised controlled trial.

INTRODUCTION: In the Chinese healthcare system, where there is overcrowding in hospitals, especially in tertiary care centres, adoption of same-day discharge (SDD) post-percutaneous coronary intervention (PCI) could potentially lead to significant savings of healthcare resources and costs. This study is a non-inferiority trial examining whether post-PCI SDD is feasible in China. The primary hypothesis is that patient outcomes in post-urgent PCI SDD patients are non-inferior to regular discharge patients. METHODS AND ANALYSIS: Post-Urgent PCI Same-DaY is an investigator-initiated multicentre randomised unblinded clinical non-inferiority trial, with 1:1 centralised randomisation to the SDD or usual care (UC) group. Based on sample size calculations, 1296 patients from at least three hospitals, with mild to moderate myocardial infarction, will be included, and acute coronary syndrome patients will be excluded. All patients will receive UC while patients assigned to the SDD group will be discharged on the same day or within 12 hours post-PCI. The primary outcome is major adverse cardiovascular and cerebrovascular events 30 days after discharge. The secondary outcomes are all-cause mortality, bleeding and access site complications. The outcome rates will be compared between groups with the absolute risk difference with a 95% CI. ETHICS AND DISSEMINATION: The study protocol V.2.0 has been approved on 21 January 2022 by the Ethics Committee of Beijing Anzhen Hospital, Capital Medical University (approval number: 2021 KLSD No. 23). The outcomes of this study will be disseminated through a peer-reviewed journal and presented at international conferences. TRIAL REGISTRATION NUMBER: ChiCTR 2200057065; China Clinical Trial Registration.

Catheter ablation of ventricular premature depolarizations originating from the mid interventricular septum: Significance of electrocardiographic morphology for predicting origin.

BACKGROUND: Ventricular premature depolarizations (VPDs) originating from the mid interventricular septum (IVS) adjacent to the atrioventricular annulus between the His bundle and the coronary sinus ostium (mid IVS VPDs) have not been characterized. OBJECTIVE: The aim of this study was to investigate the electrophysiological characteristics of mid IVS VPDs. METHODS: Thirty-eight patients with mid IVS VPDs were enrolled. VPDs were divided into different types according to precordial transition of the electrocardiogram (ECG) and QRS morphology in lead V1. RESULTS: Four types of VPDs were divided. The precordial transition zone appeared earlier and earlier from types 1 to 4. The notch in lead V1 moved gradually backward, and its amplitude gradually became higher, resulting in the transition from left to right bundle branch block morphology in lead V1 from types 1 to 4. Based on activation and pace mapping, ablation response, and 3830 electrode pacing morphology in the mid IVS, the 4 types of ECG morphology corresponded to an origin in the right endocardial side, right/mid intramural region, left intramural region, and left endocardial side of the mid IVS, respectively. An intramural origin was identified for 50% of VPDs. Eighty-nine percent of mid IVS VPDs could be eliminated. Bilateral ablation (waiting for delayed efficacy) or bipolar ablation was sometimes needed for intramural VPDs. CONCLUSION: Mid IVS VPDs were found to have unique electrophysiological characteristics. The ECG characteristics of mid IVS VPDs were important in terms of prediction of its exact origin, the choice of ablation method, and the likelihood of treatment being successful.

Case report: What course to follow when left bundle branch pacing encounters acute myocardial infarction?

Compared with traditional right ventricular apical pacing, His-bundle pacing (HBP) provides more physiologic pacing by activating the normal conduction system. However, HBP has some limitations including higher pacing thresholds. In addition, disease in the distal His-Purkinje system may prevent the correction of abnormal conduction. Left bundle branch pacing (LBBP) may overcome these disadvantages by providing lower pacing thresholds and relatively narrow QRS duration that improve cardiac function. Here, we describe a rare case of a transient loss of ventricular capture due to acute anterior wall myocardial infarction in an LBB-paced patient. With the improvement of the ischemia, the function of the pacemaker partly recovered. We review the adaptations, advantages, and limitations, and long-term safety of LBBP.

Comparison of Clinical Features at the Onset of Takayasu's Arteritis According to Age and Sex.

BACKGROUND: Takayasu's arteritis (TA) is a large-vessel vasculitis that predominantly affects the aorta, pulmonary artery, and its main branches. The cause of TA is still unclear. OBJECTIVE: To identify the clinical characteristics of TA at onset in different patient groups. METHODS: The clinical manifestations, laboratory, and angiographic findings of 53 patients with TA based on age at onset and sex were retrospectively analysed. RESULTS: The ratio of the incidence of TA in males and females was 1:4. Chest pain, reduced glomerular filtration rate (GFR), and multivessel involvement were the most common symptoms at TA onset in male patients. 17% of patients had an onset age >40 years, and the percentage of TA patients >40 years old with chest pain was significantly higher [6 (66.7%) vs 13 (29.5%) and p=0.031] than that in TA patients <40 years old. However, their renal artery involvement [1 (11.1%) vs 21 (47.7%)), p=0.042], abdominal aorta lesion [0 (0.0%) vs 16 (38.1%), p=0.030], and multiple vessel involvement [2 (22.2%) vs. 32 (72.7%), p=0.004] were significantly less evident. Multivariate analysis showed that hypertension and thoracic aortic lesion were predisposing factors for TA diagnosis [odds ratio (OR)=3.918, 95% confidence interval (CI)=1.616-1566.185, p=0.026]. For patients with aortic insufficiency (OR=3.674, 95% CI=2.734-567.621, p=0.007) or aneurysm formation (OR=7.255, 95% CI=1.23-1628.614, p=0.044), ascending aortic lesion was an independent risk factor. Furthermore, patients >40 years with chest pain but no brachial pulse should be suspected to have TA. CONCLUSION: Hypertension and thoracic aortic lesion are predisposing factors for the diagnosis of TA. Male with TA was more prone to present with chest pain, multivessel involvement, and reduced GFR.

Non-Fluoroscopic Radiofrequency Ablation of Left Atrial Appendage Tachycardia During Early Pregnancy.

Management of symptomatic atrial tachycardia (AT) during pregnancy seems challenging, especially those originating from left atrial appendage (LAA), which easily tend to be incessant and mediate cardiomyopathy. It's contradictory between therapy and pregnancy. In this study, we report a case of a woman who presented with persistent AT, which lead to heart failure, during early pregnancy. She underwent successful catheter ablation using CartoSound and electroanatomic mapping without fluoroscopy. An electrophysiology (EP) study confirmed a focal LAA tachycardia. Soon after, left ventricular function of her heart normalized, and the patient successfully delivered a healthy child.

Non-fluoroscopic radiofrequency ablation of left atrial appendage tachycardia during early pregnancy

Abstract Management of symptomatic atrial tachycardia (AT) during pregnancy seems challenging, especially those originating from left atrial appendage (LAA), which easily tend to be incessant and mediate cardiomyopathy. It's contradictory between therapy and pregnancy. In this study, we report a case of a woman who presented with persistent AT, which lead to heart failure, during early pregnancy. She underwent successful catheter ablation using CartoSound and electroanatomic mapping without fluoroscopy. An electrophysiology (EP) study confirmed a focal LAA tachycardia. Soon after, left ventricular function of her heart normalized, and the patient successfully delivered a healthy child.

Apolipoprotein-J blocks increased cell injury elicited by ox-LDL via inhibiting ROS-CaMKII pathway.

BACKGROUND: Oxidized low-density lipoprotein (ox-LDL) is crucial in cardiac injury. Apolipoprotein-J (ApoJ) contributes to antiapoptotic effects in the heart. We aimed to evaluate the protective effects of ApoJ against ox-LDL cytotoxicity in Neonatal rat ventricular cells (NRVCs). METHODS AND RESULTS: NRVCs were damaged by exposure to ox-LDL, as shown by increased caspase-3/7 activity, enhanced caspase-3 expression, and decreased cell viability. ApoJ overexpression, using an adenovirus vector, significantly reduced ox-LDL-induced cell injury. ApoJ also prevented ox-LDL from augmenting reactive oxygen species (ROS) production, as demonstrated by elevated Nox2/gp91phox and P47 expression. Furthermore, ApoJ overexpression reduced CaMKIIδ expression elicited by ox-LDL in cultured NRVCs. Upregulating CaMKIIδ activity, mediated by ox-LDL, was significantly inhibited by ApoJ overexpression. A CaMKIIδ inhibitor, KN93, prevented ApoJ's protective effect against ox-LDL cytotoxicity. A ROS scavenger, Mn (III)meso-tetrakis (4-benzoic acid) porphyrin (Mn (III)TBAP), also attenuated CaMKIIδ's increased expression and activity, induced by ox-LDL, and showed similar results to ApoJ by attenuating ox-LDL-induced cell damage, as ApoJ did. CONCLUSIONS: ApoJ confers cytoprotection to NRVCs against ox-LDL cytotoxicity through the ROS-CaMKII pathways.

Serum Levels of Inflammatory Cytokines and Expression of BCL2 and BAX mRNA in Peripheral Blood Mononuclear Cells and in Patients with Chronic Heart Failure.

BACKGROUND This study investigated the expression of the BCL2 and BAX mRNA, inflammatory cytokines, interleukin-1ß (IL-1ß), IL-6, and tumor necrosis factor-alpha (TNF-alpha), and cardiac function in patients with chronic heart failure (CHF). The New York Heart Association (NYHA) Functional Classification and measurement of the left ventricular ejection fraction (LVEF) evaluated cardiac function. MATERIAL AND METHODS Patients with CHF (n=60) due to coronary heart disease, hypertensive heart disease, and cardiomyopathy, and healthy controls (n=30) were studied. Enzyme-linked immunosorbent assay (ELISA) measured serum levels of IL-1ß, IL-6, and TNF-alpha. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) detected mRNA expression of BCL2 and BAX in peripheral blood mononuclear cells (PBMCs). Color Doppler ultrasound measured the LVEF, and the NYHA classification of CHF was used. RESULTS In patients with CHF, levels of IL-1ß, IL-6 and TNF-alpha, and mRNA expression of BAX were significantly increased compared with the control group (p<0.01); BCL2 mRNA level was significantly lower (p<0.01). There were no significant differences in the expression levels of inflammatory cytokines, or BCL2 or BAX mRNA in patients with CHF due to coronary heart disease, hypertensive heart disease, or cardiomyopathy. Expression levels of IL-1ß, IL-6, TNF-alpha, and BAX mRNA were significantly associated with the degree of CHF. Cardiac function was negatively correlated with LVEF (p<0.05). Expression levels of BCL2 mRNA level were negatively correlated with cardiac function (p<0.05), and positively correlated with LVEF (p<0.05). CONCLUSIONS Levels of IL-1ß, IL-6, TNF-alpha, and BAX mRNA were negatively correlated with cardiac function, and BCL2 mRNA expression was positively associated with CHF.

Exhaustive exercise decreases L-type calcium current by activating endoplasmic reticulum stress.

BACKGROUND: This study investigated effects of exhaustive exercise on L-type calcium current (ICa,L) and the putative intracellular cascade responsible for the effects. METHODS: Rats were randomly divided into three treatment groups: sedentary (without exercise), exercised to exhaustion and salubrinal injection before each exhaustive exercise period. Exercise group rats were forced to swim until exhaustion each time for 9 days with 5% body weight attached to the head. Salubrinal (1 mg/kg) or an equivalent volume of placebo solution (dimethyl sulfoxide) was injected via the intraperitoneal route daily for the first 3 days, followed by subcutaneous injections of salubrinal (0.5 mg/kg) or placebo solution daily for 9 days (starting 30 min before exercise). After a 1-day recovery period, whole-cell patch clamping was used to investigate the L-type Ca2+ current (ICa,L), with sedentary control rats. Additionally, endoplasmic reticulum (ER) chaperone protein levels were analyzed. RESULTS: Exhaustive exercise triggered ER stress, demonstrated by elevated expression of ER stress markers: phospho-eIF2α, CCAT/enhancer-binding homologous protein (CHOP) and caspase-12. Compared to controls, ICa,L was inhibited by exhaustive exercise, which was blocked by salubrinal, a selective eIF2α dephosphorylation inhibitor used to inhibit ER stress. These results suggest that ER stress participates in regulation of ICa,L. However, exhaustive exercise did not change the voltage dependence of steady-state activation and inactivation of ICaL, and salubrinal infusion caused no difference in voltage dependence of steady-state activation and inactivation of ICa,L. CONCLUSIONS: Exhaustive exercise activates ER stress, thus inhibiting ICaL, which may change the action potential duration and contribute to proarrhythmia.

Atorvastatin blocks increased l-type Ca2+ current and cell injury elicited by angiotensin II via inhibiting oxide stress.

Thel-type Ca(2+)current (ICa,l) plays a crucial role in shaping action potential and is involved in cardiac arrhythmia. Statins have been demonstrated to contribute to anti-apoptotic and anti-arrhythmic effects in the heart. Here, we examined whether atorvastatin regulates theICa,land cell injury induced by angiotensin II (AngII) as well as the putative intracellular cascade responsible for the effects. Cultured neonatal rat ventricular myocytes were incubated with AngII for 24 h, and then cell injury and expression levels of Nox2/gp91(phox), p47(phox) ,and Cav1.2 were analyzed. In addition,ICa,lwas recorded using the whole-cell patch-clamp technique, and mechanisms of atorvastatin actions were also investigated. It was found that the number of apoptotic cardiomyocytes was increased and cell viability was significantly decreased after AngII administration. AngII also augmented the expressions of Nox2/gp91(phox)and p47(phox)compared with control cardiomyocytes. Exposure to AngII evokedICa,lin a voltage-dependent manner without affecting theI-Vrelationship. In addition, AngII enhanced membrane Cav1.2 expression. These effects were abolished in the presence of the reactive oxygen species (ROS) scavenger, manganese (III)-tetrakis 4-benzoic acid porphyrin [Mn(III)TBAP], or the 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor, atorvastatin. These results suggested that atorvastatin mediates cardioprotection against arrhythmias and cell injury by controlling the AngII-ROS cascade.

Apolipoprotein-J prevents angiotensin II-induced apoptosis in neonatal rat ventricular cells.

BACKGROUND: Up-regulation of angiotensin II (AngII) occurs in cardiac diseases, such as congestive heart failure, cardiac hypertrophy, myocardial ischemia and atrial fibrillation, which represent major health problems. Evidence from in vivo studies suggests that the level of Apolipoprotein-J (ApoJ) is also elevated but plays a protective role in cardiovascular disease. This study aimed to evaluate the protective effects of ApoJ against cytotoxicity of AngII in neonatal rat ventricular cells (NRVCs). METHODS AND RESULTS: In culture, NRVCs were damaged by exposure to AngII, and ApoJ overexpression using an adenovirus vector significantly reduced the AngII-induced cell injury. ApoJ also prevented AngII from augmenting Nox2/gp91(phox) expression. The reactive oxygen species (ROS) scavenger, Mn(III)TBAP, showed similar results of attenuating AngII-induced cell damage. Furthermore, ApoJ overexpression increased phosphorylation of Akt, and the phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 diminished the antioxidant effects of ApoJ, and prevented the protective effect of ApoJ against the cytotoxicity of AngII. Moreover, upregulation of nuclear factor κB (NF-κB) p65 expression and phosphorylation of p38 mitogen-activated protein kinase (MAPK) mediated by AngII in cultured NRVCs were significantly inhibited by overexpression of ApoJ. The p38 MAPK inhibitor SB203580 and the NF-κB inhibitor PDTC protected NRVCs from injury caused by AngII. CONCLUSIONS: ApoJ serves as a cytoprotective protein in NRVCs against cytotoxicity of AngII through the PI3K-Akt-ROS and MAPK/ NF-κB pathways.

Reduced endoplasmic reticulum stress might alter the course of heart failure via caspase-12 and JNK pathways.

BACKGROUND: Endoplasmic reticulum (ER) stress plays an important role in mediating ischemic heart cell death. The aim of this study was to investigate whether manipulation of a key factor of the ER stress pathway, eukaryotic translation initiation factor 2 subunit α (eIF2α), can change the natural history of heart failure (HF). METHODS: HF was induced using coronary artery ligation in adult rats and a selective eIF2α dephosphorylation inhibitor, salubrinal (Sal), was used. Thirty minutes after ligation, rats were randomly assigned to 3 groups: myocardial infarction (MI) plus placebo injections (dimethyl sulfoxide; n = 12), MI plus Sal injection (Sal; n = 12), and MI (HF; n = 12). Hemodynamic parameters were examined. Hearts were harvested for apoptosis assessment after 8 weeks of Sal treatment by terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labelling and flow cytometric analysis. Hearts were harvested to determine ER chaperones by Western analysis, real-time polymerase chain reaction and immunohistochemical analysis. RESULTS: Cardiac function was significantly improved in Sal-treated rats. Apoptosis was reduced by Sal treatment. Glucose-regulated protein-78 and -94 were increased in HF but normalized by Sal treatment. HF caused a significant increase in eIF2α phosphorylation, which was further increased by Sal treatment, and caspase-12 and phospho-c-JUN NH2-terminal kinase were markedly increased in rats with HF alone but significantly reduced by Sal treatment. CONCLUSIONS: Our results suggest that reduction of ER stress and myocardial apoptosis through inhibition of eIF2α dephosphorylation might alter the natural history of HF, which might provide a new approach for its treatment.

[Analyses of super-response to cardiac resynchronization therapy in patients with congestive heart failure: a multiple center trial].

OBJECTIVE: To evaluate the incidence of super-response and the potential predictors related to super-response after cardiac resynchronization therapy (CRT) in patients with congestive heart failure. METHODS: 190 patients [145 men and 45 women;age: (60.48 ± 11.91) years] underwent CRT between March 2001 and March 2012 were enrolled in this multi-center trial, of which, 54 patients with ischemic cardiomyopathy and 136 patients with non-ischemic cardiomyopathy. These patients were followed up from 6 months to 11 years (mean 58 months) post CRT. RESULTS: Ten patients died within 6 months post CRT, the others were followed up for more than 6 months. At 6-month follow-up, 51 patients were identified as CRT super-responders (28.33%), 75 patients were CRT responders (41.67%) and 29 patients were CRT non-responders (16.11%), and 25 patients were CRT negative responders (13.89%). Super-response occurred more frequently in non-ischemic cardiomyopathy patients, while non-response most commonly occurred in ischemic cardiomyopathy patients (P < 0.05); patients in the negative response group had higher serum creatinine level than other groups (P < 0.05) , and patients in the non-response group and negative response group had higher pulmonary artery pressure than patients in the super-response group (P < 0.05); the average QRS duration was ≥ 160 ms before CRT, and the mean decrease was around 30 ms after CRT in the super-response group while the average QRS duration was 139 ms before CRT, and the mean reduction was around 8 ms after CRT in the negative response group (P < 0.05). LV lead position in the super-response group was usually in the middle and base of the heart, while in the negative response group it was more commonly located in the apex of the heart (P < 0.01) . CONCLUSIONS: LV lead located at the middle and pre-CRT ORS duration ≥ 160 ms are associated with super-response post CRT procedure in this patient cohort.

[Causes of non-response to cardiac resynchronization therapy in heart failure patients with permanent atrial fibrillation].

OBJECTIVE: To evaluate the long-term effects and analyze causes of non-response to cardiac resynchronization therapy (CRT) in heart failure (HF) patients with permanent atrial fibrillation (AF). METHODS: Thirty-three patients with HF and AF [29 men, mean age (61 ± 10) years, NYHA class III or IV, left ventricular ejection fraction (LVEF) ≤ 35%, QRS ≥ 120 ms in 31 cases] underwent bi-ventricular pacing (n = 26) or bi-ventricular pacing and atrioventricular node ablation (AVN-ablation, n = 7) were included in this study. Non-response was defined: the increase of left ventricular ejection fraction (LVEF) was less than 15%. Patients were followed-up for 4 years. RESULTS: Six patients died during follow up. Non-responder to CRT was observed in 6 out of 27 survived patients (22.22%). Six out of 7 patients underwent AVN-ablation were in responder group and 1 in non-responder group. Comparing with responder group, the baseline LVEF was significantly higher (37% vs. 32%, P = 0.003), and the history of HF was significantly longer (6.3 years vs. 4.1 years, P = 0.039), pulmonary artery pressure was significantly higher (53 vs. 32 mm Hg, P = 0.027), bi-ventricular pacing percentage (BIVP%) was significantly lower (75.86% vs. 91.73%, P = 0.007) in non-responder group. CONCLUSIONS: Higher LVEF, longer HF history, higher pulmonary artery pressure and lower BIVP% are factors linked with non-responses to CRT in this patient cohort. CRT plus AVN-ablation is associated with high response rate to CRT in this patient cohort.

[The mechanistic rote of KCNH2 gene L413P and L559H mutations in long QT syndrome].

OBJECTIVE: To investigate the molecular pathogenesis for two novel mutations L413P and L559H of KCNH2 found in Chinese patients with long QT syndrome. METHODS: L413P and L559H mutant constructs were generated by site-directed mutagenesis using human wild-type (WT) pcDNA3-HERG cDNA as a template. WT and mutant constructs were transiently transfected into human embryonic kidney 293 cells using lipofectamine method. After transfection, the recording of HERG current was performed using patch clamp technique. The expression and cellular localization of HERG protein were studied with Western blot and immunofluorescence methods. RESULTS: Electrophysiological recordings showed that L413P and L559H mutations did not express HERG current. Western blot analysis revealed that only 135 000 immature HERG protein was expressed in L413P and L559H-transfected cells, whereas both mature and immature forms of HERG protein were observed in WT-transfected cells. Immunofluorescence study showed that L413P and L559H mutant proteins were predominantly localized around the nucleus, suggesting that the mutant channels are retained in the endoplasmic reticulum. When L413P or L559H was co-transfected with equal amount of WT plasmids, both 135 000 and 155 000 forms of HERG protein were observed, and the HERG current was not significantly changed as compared with that of WT transfection alone. Low temperature and E-4031could not rescue these two mutant channels. CONCLUSIONS: The L413P and L559H mutations resulted in protein trafficking defects with failure of mutant proteins to reach the plasma membrane. However, both biochemical and electrophysiological results showed that the mutations did not have a dominant-negative effect on WT, indicating that the mechanism of the L413P and L559H mutations might be haploinsufficiency.

Expression and clinical significance of vascular endothelial growth factor, cyclooxygenase-2, and Bcl-2 in borderline ovarian tumors.

OBJECTIVE: The objectives were to study the expression of vascular endothelial growth factor (VEGF), cyclooxygenase-2 (Cox-2), and Bcl-2 in borderline ovarian tumors (BOTs) and the relationship within them, and to investigate the correlation between expression of VEGF, Cox-2, and Bcl-2, and the clinicopathologic features of BOTs. METHODS: An immunohistochemical technique was used to investigate the expression of VEGF ,Cox-2, and Bcl-2 in 69 borderline, 18 benign, and 27 malignant human ovarian tumor tissues. RESULTS: Expression rate of VEGF protein (59.4%) in BOTs was higher than in benign tumors (27.8%) and was lower than in ovarian carcinomas (92.6%), and there was a significant difference between BOTs and benign ovarian tumors (p < 0.05), and carcinoma (p < 0.01). Significant correlation was observed between the positive expression rate for VEGF and clinical stage of BOTs (p < 0.05). The statistical analysis did not show a close correlation between the expression of VEGF and tissue type, and peritoneal implants in BOTs (p > 0.05). The expression rate of Cox-2 was significantly higher in ovarian carcinomas (81.5%) than in BOTs (57.9%) and in benign ovarian tumors (38.9%) (p < 0.05). Significant correlation was observed between the positive expression rate for Cox-2 and the clinical stage of BOTs (p < 0.05). The statistical analysis showed no close correlation between the expression of Cox-2 and tissue type, and peritoneal implants in BOTs (p > 0.05). There was a significant difference between the expression of Bcl-2 in ovarian carcinomas and BOTs than that in benign ovarian tumors (p < 0.05). The positive expression rate of Bcl-2 was not related to clinical stages and peritoneal implants (p > 0.05). Statistical analysis showed a positive correlation between the expression of Cox-2 and VEGF, and Bcl-2 in BOTs. CONCLUSIONS: Overexpression of VEGF, Cox-2, and Bcl-2 in BOTs may play an important role in the oncogenesis and progression of BOTs. It is feasible to detect VEGF, Cox-2, and Bcl-2 in the diagnosis and to predict the prognosis of BOTs.

[Effect of simulated ischemia on activity and heterogeneity of Na+ channel in rabbit ventricular epicardial, midmyocardial and endocardial myocytes].

OBJECTIVE: To study the ionic mechanism of reentrant arrhythmia. METHODS: Single myocytes were enzymatically isolated from the epicardium, midmyocardium and endocardium of the left ventricle free wall of rabbit, followed by whole-cell patch-clamp recording of the Na(+) current (I(Na)) of the 3 cellular subtypes (superfused with normal and then simulated ischemia solution). The currents in the 3 cellular subtypes before and after simulated ischemia lasting for 10, 20, and 30 min, respectively, were compared. RESULTS: No changes was recorded in the configuration of the I-V curves and voltage dependence of I(Na) after simulated ischemia, and the peak I(Na) densities (- 20 mV) were significantly reduced in the 3 cellular subtypes compared with those recorded in normal condition. At the same time, the differences in I(Na) peak current densities in the 3 cellular subtypes underwent variations after simulated ischemia. Simulated ischemia resulted in obvious shift of I(Na) steady-state inactivation curves in the hyperpolarizing direction in the 3 cellular subtypes and inactivation was accelerated, and the differences in the half maximal inactivation voltages (V0.5) between the 3 cellular subtypes were also altered after simulated ischemia. After simulated ischemia, I(Na) recovery from inactivation in the epicardium, endocardium and midmyocardium was all slowed down in comparison with that in normal condition, but without statistical significance. Differences between the recovery curves of three cellular subtypes were noted after ischemia for 30 min. CONCLUSION: Ischemia can affect the activity of Na(+) channel, disrupting the balance of ion channel currents and the heterogeneity of I(Na) among the 3 cellular subtypes, which is responsible for the onset of arrhythmia and partially explains different pharmacological reactions of the 3 cellular subtypes under normal and ischemic conditions.