Surgical treatment of multivalvular endocarditis: Twenty-one–year single center experience

ObjectiveLittle information is available about surgical outcomes in patients with multivalvular endocarditis. The aim of this article is to review the 21-year experience with surgical treatment of patients with multivalvular endocarditis at our institution and, in particular, to determine the incidence, pathologic status, diagnosis, surgical strategies, and outcomes of patients with this disease.MethodsFrom January 1986 to December 2006, a total of 48 patients (40 men, 8 women), with a mean age of 42 ± 12 years, underwent surgery for multivalvular endocarditis. Endocarditis was active in 32 patients and healed in 16. Preoperative transthoracic echocardiographic evaluation was performed in all 48 patients with addition of transesophageal echocardiography in 22 (45.8%). Intraoperative findings showed that the endocarditis involved mostly the mitral and aortic valves (40/48 patients). Triple or quadruple valve involvement was found in 1 and 2 patients, respectively. Preoperative, perioperative, and postoperative data were retrospectively analyzed and risk factors for early and late survival were determined.ResultsIn only 24 (50.0%) patients was multivalvular endocarditis diagnosed by preoperative transthoracic echocardiography; 17 (77.3%) patients had multivalvular endocarditis confirmed by preoperative transesophageal echocardiography. The 30-day hospital mortality was 12.5% (n = 6). Preoperative renal failure, New York Heart Association class IV, and emergency surgery were identified as independent risk factors for hospital mortality. Overall long-term survival was 74% ± 6% at 5 years and 62% ± 3% at 10 years. Multivariate analysis revealed that renal failure and recurrent endocarditis were associated with increased late mortality. Ten-year freedom from recurrent endocarditis was 74% ± 5% and 10-year freedom from reoperation was 73% ± 6%.ConclusionsIn our institution, multivalvular endocarditis was diagnosed by transthoracic echocardiography in only half of the patients. Intraoperative transesophageal echocardiography provided a more effective means to identify this disease. Radical resection of all infected tissues for patients with multivalvular endocarditis and additional intraoperative interventions, depending on the intraoperative pathologic condition, produced satisfactory in-hospital and long-term results, similar to those in patients with a single infected heart valve

2-(4-Bromo­phen­yl)quinoxaline

In the title compound, C14H9BrN2, the benzene and quinoxaline rings are almost coplanar [r.m.s. deviation = 0.0285 (3) Å and dihedral angle = 2.1 (2)°]

CCR2 expression correlates with prostate cancer progression

Although the primary role of chemokines and their receptors is controlling the trafficking of leukocytes during inflammatory responses, they also play pleoitropic roles in cancer development. There is emerging evidence that cancer cells produce chemokines that induce tumor cell proliferation or chemotaxis in various cancer types. We have previously reported that MCP-1 acts as a paracrine and autocrine factor for prostate cancer (PCa) growth and invasion. As the cellular effects of MCP-1 are mediated by CC chemokine receptor 2 (CCR2), we hypothesized that CCR2 may contribute PCa progression. Accordingly, we first determined CCR2 mRNA and protein expression in various cancer cell lines, including PCa and other cancer types. All cells expressed CCR2 mRNA and protein, but in PCa, more aggressive cancer cells such as C4-2B, DU145, and PC3 expressed a higher amount of CCR2 compared with the less aggressive cancer cells such as LNCaP or non-neoplastic PrEC and RWPE-1 cells. Further, we found a positive correlation between CCR2 expression and PCa progression by analyzing an ONCOMINE gene array database. We confirmed that CCR2 mRNA was highly expressed in PCa metastatic tissues compared with the localized PCa or benign prostate tissues by real-time RT-PCR. Finally, CCR2 protein expression was examined by immunohistochemical staining on tissue microarray specimens from 96 PCa patients and 31 benign tissue controls. We found that CCR2 expression correlated with Gleason score and clinical pathologic stages, whereas lower levels of CCR2 were expressed in normal prostate tissues. These results suggest that CCR2 may contribute to PCa development. J. Cell. Biochem. 101: 676–685, 2007. © 2007 Wiley-Liss, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/56008/1/21220_ftp.pd

Gemcitabine enhances cell invasion via activating HAb18G/CD147-EGFR-pSTAT3 signaling

Pancreatic cancer, one of the most lethal cancers, has very poor 5-year survival partly due to gemcitabine resistance. Recently, it was reported that chemotherapeutic agents may act as stressors to induce adaptive responses and to promote chemoresistance in cancer cells. During long-term drug treatment, the minority of cancer cells survive and acquire an epithelial-mesenchymal transition phenotype with increased chemo-resistance and metastasis. However, the short-term response of most cancer cells remains unclear. This study aimed to investigate the short-term response of pancreatic cancer cells to gemcitabine stress and to explore the corresponding mechanism. Our results showed that gemcitabine treatment for 24 hours enhanced pancreatic cancer cell invasion. In gemcitabine-treated cells, HAb18G/CD147 was up-regulated; and HAb18G/CD147 down-regulation or inhibition attenuated gemcitabine-enhanced invasion. Mechanistically, HAb18G/CD147 promoted gemcitabine-enhanced invasion by activating the EGFR (epidermal growth factor receptor)-STAT3 (signal transducer and activator of transcription 3) signaling pathway. Inhibition of EGFR-STAT3 signaling counteracted gemcitabine-enhanced invasion, and which relied on HAb18G/CD147 levels. In pancreatic cancer tissues, EGFR was highly expressed and positively correlated with HAb18G/CD147. These data indicate that pancreatic cancer cells enhance cell invasion via activating HAb18G/CD147-EGFR-pSTAT3 signaling. Our findings suggest that inhibiting HAb18G/CD147 is a potential strategy for overcoming drug stress-associated resistance in pancreatic cancer

Triple Flares within Five Years in ztf18aanlzzf: An Enhanced Tidal Disruption Rate in ULIRGs?

We present a noteworthy transient event in the optical light curves of ztf18aanlzzf (SDSS J161259.83+421940.3), identified as a Narrow Line Seyfert 1 (NLS1) exhibiting merging patterns in the optical image. The 16-year long-term archived light curve revealed that this target stays in a steady state, while three flares occurred within the past 5 years with time separations ranging from 1 year to 3.5 years. The flare patterns of rapid brightening and slow decline following the peak, coupled with distinctive spectral features with strong He {\sc ii} and rare appearance of Bowen fluorescence line emissions, indicate at least two Tidal Eruption Event (TDE) flares in ztf18aanlzzf with a time separation of 3.5 years. We also apply TiDE light curve modeling and yield a Black Hole (BH) mass of $\sim 10^{6}\ M_{\odot}$, which is consistent with the BH mass measured from single-epoch spectra. Besides, the observed time lags $3.90_{-2.00}^{+2.06}$ days between the g and r bands strongly disagree with the prediction of the standard accretion disk model, highlighting the intricate interaction in the inner region related to the TDE. The reoccurrence gap of these TDEs, surpassing the previously reported repeated TDEs, can be attributed to binary star tidal disruption by a binary SMBH. Notably, the frequent TDE flares observed in this ULIRG-like target align with findings in a previous report for another ULIRG, suggesting a potentially elevated TDE rate in ULIRGs. Systematic variability studies of ULIRGs may help verify whether ULIRGs indeed have higher TDE rates.Comment: 10 pages, 4 figures, submitte