694 research outputs found
Reply to "The impact of nerve sparing robotic-assisted radical prostatectomy on positive surgical margins: Uncertainty"
Effects of nerve-sparing procedures on surgical margins after robot-assisted radical prostatectomy
BACKGROUND: Nerve-sparing (NS) techniques could potentially increase positive surgical margins (PSM) after robot-assisted radical prostatectomy (RARP). Nevertheless, the available studies have revealed ambiguous results among distinct groups. This study purposed to clarify the details of NS techniques to accurately estimate their influence on margin status. METHODS: We studied RARPs performed by one surgeon from 2010 to 2018. Surgical margins were evaluated by the laterality and levels of NS techniques in site-specific prostate lobes. The multivariable analysis evaluated the effects of nerve-sparing procedures, combined with other covariate factors, on margin status. RESULTS: Overall, four hundred nineteen RARPs involving 838 prostate lobes were analyzed. Notably, 181 patients (43.4%) had pT2-stage, and 236 (56.6%) had pT3-stage cancer. The PSM rates for patients who underwent unilateral, bilateral, and non NS procedures were 30.3%, 28.8%, and 50%, respectively (p = 0.233) or in stratification by pT2 (p = 0.584) and pT3 (p = 0.116) stage. The posterolateral PSM rates among site-specific prostate lobes were 10.9%, 22.4%, and 18.9% for complete, partial, and non NS techniques, respectively (p = 0.001). The partial NS group revealed a significant increase in PSM rate compared with the complete NS (OR 2.187, 95% CI 1.19-4.03) and non NS (OR 2.237, 95% CI 1.01-4.93) groups in site-specific prostate lobes. CONCLUSION: Partial NS procedures have a potential risk of increasing the PSM rate than complete and non NS procedures do. Therefore, correct case selection is required before performing partial NS techniques
Unusual dyspnea in a hemodialysis patient: A case report
The typical clinical symptoms of hemothorax include a rapid development of chest pain or dyspnea, which may be life-threatening without immediate management. As we know, spontaneous hemothorax, a collection of blood within the pleural cavity without previous history of trauma or other cause, which usually onsets suddenly. The early and accurate diagnosis of spontaneous hemothorax is imperative in clinical practice. We reported a middle-age male undergoing regular hemodialysis was referred to our emergency department due to unknown cause of dyspnea and acute respiratory failure. Chest radiography revealed bilateral patchy infiltration of lung. Pleural tap analysis showed exudative pleural effusion with numerous red blood cells. Video-assisted thoracic surgery (VATS) were performed and confirmed the final diagnosis of spontaneous hemothorax. He was then successfully treated with the surgery of VATS combined chest tube thoracostomy
The nucleolar protein NIFK promotes cancer progression via CK1α/β-catenin in metastasis and Ki-67-dependent cell proliferation.
Nucleolar protein interacting with the FHA domain of pKi-67 (NIFK) is a Ki-67-interacting protein. However, its precise function in cancer remains largely uninvestigated. Here we show the clinical significance and metastatic mechanism of NIFK in lung cancer. NIFK expression is clinically associated with poor prognosis and metastasis. Furthermore, NIFK enhances Ki-67-dependent proliferation, and promotes migration, invasion in vitro and metastasis in vivo via downregulation of casein kinase 1α (CK1α), a suppressor of pro-metastatic TCF4/β-catenin signaling. Inversely, CK1α is upregulated upon NIFK knockdown. The silencing of CK1α expression in NIFK-silenced cells restores TCF4/β-catenin transcriptional activity, cell migration, and metastasis. Furthermore, RUNX1 is identified as a transcription factor of CSNK1A1 (CK1α) that is negatively regulated by NIFK. Our results demonstrate the prognostic value of NIFK, and suggest that NIFK is required for lung cancer progression via the RUNX1-dependent CK1α repression, which activates TCF4/β-catenin signaling in metastasis and the Ki-67-dependent regulation in cell proliferation
The Study on Antecedents of Consumer Buying Impulsiveness in an Online Context
The global recession caused by the financial tsunami has seriously impacted numerous industries. Although the market scale of global e-commerce market has declined, global online shopping continues to grow. Many previous researches focused on the effect of website design characteristics on online impulsive buying behavior, and few have explored such behavior from consumer individual internal factor perspectives. This paper aims to explore and integrate individual internal factors influencing consumer online buying impulsiveness, and further to recognize the relationships among these factors. The results showed as follows: (1) hedonic consumption needs, impulsive buying tendency, positive affect and normative evaluations positively influence buying impulsiveness, respectively; (2) hedonic consumption needs positively influence positive affect; (3) impulsive buying tendency positively influences normative evaluations; (4) normative evaluations positively influence positive affect
Regulation of shear-induced nuclear translocation of the Nrf2 transcription factor in endothelial cells
<p>Abstract</p> <p>Background</p> <p>Vascular endothelial cells (ECs) constantly experience fluid shear stresses generated by blood flow. Laminar flow is known to produce atheroprotective effects on ECs. Nrf2 is a transcription factor that is essential for the antioxidant response element (ARE)-mediated induction of genes such as heme-oxygenase 1 (HO-1). We previously showed that fluid shear stress increases intracellular reactive oxygen species (ROS) in ECs. Moreover, oxidants are known to stimulate Nrf2. We thus examined the regulation of Nrf2 in cultured human ECs by shear stress.</p> <p>Results</p> <p>Exposure of human umbilical vein endothelial cells (HUVECs) to laminar shear stress (12 dyne/cm<sup>2</sup>) induced Nrf2 nuclear translocation, which was inhibited by a phosphatidylinositol 3-kinase (PI3K) inhibitor, a protein kinase C (PKC) inhibitor, and an antioxidant agent N-acetyl cysteine (NAC), but not by other protein kinase inhibitors. Therefore, PI3K, PKC, and ROS are involved in the signaling pathway that leads to the shear-induced nuclear translocation of Nrf2. We also found that shear stress increased the ARE-binding activity of Nrf2 and the downstream expression of HO-1.</p> <p>Conclusion</p> <p>Our data suggest that the atheroprotective effect of laminar flow is partially attributed to Nrf2 activation which results in ARE-mediated gene transcriptions, such as HO-1 expression, that are beneficial to the cardiovascular system.</p
Continuous Production of Lipase-Catalyzed Biodiesel in a Packed-Bed Reactor: Optimization and Enzyme Reuse Study
An optimal continuous production of biodiesel by methanolysis of soybean oil in a packed-bed reactor was developed using immobilized lipase (Novozym 435) as a catalyst in a tert-butanol solvent system. Response surface methodology (RSM) and Box-Behnken design were employed to evaluate the effects of reaction temperature, flow rate, and substrate molar ratio on the molar conversion of biodiesel. The results showed that flow rate and temperature have significant effects on the percentage of molar conversion. On the basis of ridge max analysis, the optimum conditions were as follows: flow rate 0.1 mL/min, temperature 52.1°C, and substrate molar ratio 1 : 4. The predicted and experimental values of molar conversion were 83.31 ± 2.07% and 82.81 ± .98%, respectively. Furthermore, the continuous process over 30 days showed no appreciable decrease in the molar conversion. The paper demonstrates the applicability of using immobilized lipase and a packed-bed reactor for continuous biodiesel synthesis
Characterization of pulmonary protein profiles in response to zinc oxide nanoparticles in mice: a 24-hour and 28-day follow-up study
Although zinc oxide nanoparticles (ZnONPs) are recognized to cause systemic disorders, little is known about the mechanisms that underlie the time-dependent differences that occur after exposure. The objective of this study was to investigate the mechanistic differences at 24 hours and 28 days after the exposure of BALB/c mice to ZnONPs via intratracheal instillation. An isobaric tag for the relative and absolute quantitation coupled with liquid chromatography/tandem mass spectrometry was used to identify the differential protein expression, biological processes, molecular functions, and pathways. A total of 18 and 14 proteins displayed significant changes in the lung tissues at 24 hours and 28 days after exposure, respectively, with the most striking changes being observed for S100-A9 protein. Metabolic processes and catalytic activity were the main biological processes and molecular functions, respectively, in the responses at the 24-hour and 28-day follow-up times. The glycolysis/gluconeogenesis pathway was continuously downregulated from 24 hours to 28 days, whereas detoxification pathways were activated at the 28-day time-point after exposure. A comprehensive understanding of the potential time-dependent effects of exposure to ZnONPs was provided, which highlights the metabolic mechanisms that may be important in the responses to ZnONP
Evaluation of the immunological functions of placental alkaline phosphatase in vivo using ALPP transgenic mice
Alkaline phosphatase (ALP) is a ubiquitously expressed dephosphorylating enzyme and its level in blood is widely used as a diagnosis marker of liver damage or bone disorders in human patients. ALP is also considered as an anti-inflammatory protein due to its ability to dephosphorylate and inactivate inflammation-triggering molecules such as lipopolysaccharide (LPS). Placental alkaline phosphatase (ALPP) is one of tissue-specific ALP isozymes expressed mostly during pregnancy, however it was found to be differentially upregulated in certain hepatocellular carcinomas by us recently. In addition, ALPP has been identified as a reliable biomarker of diverse germ cell tumors. Nevertheless, little is known of its immune modulatory role in vivo. In this study, we generated ALPP transgenic mice and tested these mice in the LPS-induced sepsis and male-to-female skin graft rejection models. Our results showed that ALPP transgenic mice are more susceptible to intraperitoneal injection of LPS in comparison to control animals. In addition, female ALPP transgenic mice were better at delaying the rejection of male skin grafts. In an in vitro phagocytosis experiment, addition of exogenous ALPP compromised the phagocytic ability of THP-1 monocytic cells. These results indicate that excess ALPP plays a role in modulating both innate and adaptive immune functions
Identification of novel DNA methylation inhibitors via a two-component reporter gene system
<p>Abstract</p> <p>Background</p> <p>Targeting abnormal DNA methylation represents a therapeutically relevant strategy for cancer treatment as demonstrated by the US Food and Drug Administration approval of the DNA methyltransferase inhibitors azacytidine and 5-aza-2'-deoxycytidine for the treatment of myelodysplastic syndromes. But their use is associated with increased incidences of bone marrow suppression. Alternatively, procainamide has emerged as a potential DNA demethylating agent for clinical translation. While procainamide is much safer than 5-aza-2'-deoxycytidine, it requires high concentrations to be effective in DNA demethylation in suppressing cancer cell growth. Thus, our laboratories have embarked on the pharmacological exploitation of procainamide to develop potent DNA methylation inhibitors through lead optimization.</p> <p>Methods</p> <p>We report the use of a DNA methylation two-component enhanced green fluorescent protein reporter system as a screening platform to identify novel DNA methylation inhibitors from a compound library containing procainamide derivatives.</p> <p>Results</p> <p>A lead agent IM25, which exhibits substantially higher potency in <it>GSTp1 </it>DNA demethylation with lower cytotoxicity in MCF7 cells relative to procainamide and 5-aza-2'-deoxycytidine, was identified by the screening platform.</p> <p>Conclusions</p> <p>Our data provide a proof-of-concept that procainamide could be pharmacologically exploited to develop novel DNA methylation inhibitors, of which the translational potential in cancer therapy/prevention is currently under investigation.</p
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