[Effect of L-Type Amino Acid Transporter 1 Expression on Clinicopathological Features and Prognosis of Non-Hodgkin's Lymphoma].

OBJECTIVE: To detect the expression of L-type amino acid transporter 1 (LAT1) in non-Hodgkin's lymphoma (NHL) tissues, and analyze its effect on clinicopathological characteristics and prognosis of patients. METHODS: A total of 92 NHL patients who were treated in our hospital from January 2017 to April 2019 were collected. The expression of LAT1 in NHL tissue was detected by immunohistochemistry and compared between patients with different pathological features (including sex, Ann Arbor stage, extranodal infiltration, Ki-67). The risk factors affecting mortality were analyzed using univariate and multivariate Cox proportional hazards regression. Receiver operating characteristic (ROC) curve was used to detect the predictive value of percentage of LAT1-positive cells in NHL tissue for patient mortality, and analyzing the effect of percentage of LAT1-positive cells on survival rate. RESULTS: LAT1 was positively expressed in NHL tissue. The high expression rate of LAT1 in Ann Arbor stage III and IV groups were higher than that in Ann Arbor stage I group, that in extranodal infiltration group was higher than non-extranodal infiltration group, and that in Ki-67 positive expression group was higher than Ki-67 negative expression group (all P < 0.05). The remission rate after 3 courses of treatment in high-LAT1 expression group was 70.7%, which was lower than 91.2% in low-LAT1 expression group (P < 0.05). Ann Arbor stage III and IV, extranodal invasion, Ki-67 positive expression and increased expression of LAT1 (LAT1-positive cell percentage score ≥2) were risk factors for mortality. The cut-off value of percentage of LAT1-positive cells for predicting NHL death was 45.6%, and the area under the ROC curve was 0.905 (95%CI: 0.897-0.924). The 3-year survival rate of high-LAT1 level group (the percentage of LAT1-positive cells≥45.6%) was 50.00%, which was lower than 78.26% of low-LAT1 level group (P < 0.05). CONCLUSION: The expression level of LAT1 in NHL tissue increases, which affects Ann Arbor stage and extranodal infiltration of patients. LAT1 is a risk factor for death.

Effects of instantaneous changes in temperature, light, and salinity on the dynamics of dissolved organic carbon release by Sargassum thunbergii.

Although macroalgae are regarded as the emerging fourth category of "blue carbon", few studies are available on the dynamics of dissolved organic carbon (DOC) release. Sargassum thunbergii is a typical intertidal macroalgae; and tidal action usually triggers instantaneous changes in temperature, light and salinity. Therefore, we investigated the mechanism of short-term changes in temperature, light and salinity on DOC release by S. thunbergii. As well as these factors coupled with desiccation, the combined effect of DOC release was revealed. The results showed the DOC release rate of S. thunbergii was from 0.028 to 0.037 mg C g -1(FW) h-1 under different photosynthetically active radiation (PAR, 0-1500 µmol photons m-2 s-1). The DOC release rate of S. thunbergii was from 0.008 to 0.208 mg C g -1(FW) h-1 under different salinity (5-40). The DOC release rate of S. thunbergii was from 0.031 to 0.034 mg C g -1(FW) h-1 under different temperature (10-30 °C). Either the increase in intracellular organic matter concentration due to increased photosynthesis (change in PAR and temperature, active), cell dehydration due to dry-out process (passive) or the decrease in extracellular salt concentration (passive) would lead to an increase in the difference in osmotic pressure and promote DOC release.

Role of Vitamin C in Cardioprotection of Ischemia/Reperfusion Injury by Activation of Mitochondrial KATP Channel.

How to provide effective prevention and treatment of myocardial ischemia/reperfusion (I/R) injury and study of the mechanism underlying I/R injury are hotspots of current research. This study aimed to elucidate the effect and cardioprotective mechanism of vitamin C (VC) on myocardial I/R injury. Our study introduced two different I/R models: I/R in vitro and oxygen-glucose deprivation/recovery (OGD/R) in primary neonatal rat cardiac myocytes. We used the mitochondrial permeability transition pore (mPTP) opener lonidamine (LND) and the mitochondrial KATP (mitoKATP) channel inhibitor 5-hydroxydecanoate (5-HD) to analyze the underlying mechanisms. We found that post-treatment with VC decreased I/R injury in our models. Post-treatment with VC significantly decreased I/R-induced injury, attenuated apoptosis, and maintained the functional integrity of mitochondria via alleviation of Ca(2+) overload, reactive oxygen species burst, inhibition of the opening of mPTP, and prevention of mitochondrial membrane potential (ΔΨm) depolarization. VC post-treatment increased the phosphorylation of Akt and glycogen synthase kinase (GSK)-3ß. The present results demonstrate that VC might protect the myocardium from I/R-induced injury by inhibiting the mPTP opening via activation of mitoKATP channels. VC mediates cardioprotection via activation of the phosphatidyl inositol 3-kinase (PI3K)-Akt signaling pathway. These findings may contribute toward the development of novel strategies for clinical cardioprotection against I/R injury.

Acortatarin A inhibits high glucose-induced extracellular matrix production in mesangial cells.

BACKGROUND: Diabetic nephropathy (DN) is the leading cause of end-stage renal disease. Various treatment regimens and combinations of therapies provide only partial renoprotection. Therefore new approaches are needed to retard the progression of DN. The aim of the present study was to evaluate the role of a novel spiroalkaloid from Acorus tatarinowii named acortatarin A (AcorA) in inhibiting high glucose-induced extracellular matrix accumulation in mesangial cells (MCs). METHODS: The cytotoxity of AcorA on MCs was examined by 3-(4,5-dimethylthiazol-2-yl)-2.5-diphenyltetrazolium bromide (MTT) assay. The expression of fibronectin and collagen IV was examined by real time PCR and western blotting. The expression of p22(phox) and p47(phox) was detected by western blot. The interaction between p22(phox) and p47(phox) was examined by co-immunoprecipitation. The phosphorylation of p47(phox) was examined by immunoprecipitation. The phosphorylation of protein kinase C (PKC) α, PKCß, phospholiase C gamma (PLCγ1), and the p85 subunit of PI3K was determined by Western blotting. RESULTS: AcorA significantly inhibited high glucose-induced activation of NADPH oxidase, a ROS-generating enzyme, by increasing phosphorylation of p47(phox) and enhancing interaction between p22(phox) and p47(phox). Preincubation of AcorA with MCs inhibited high glucose-induced collagen IV and fibronectin production in a dose-dependent manner. Moreover, AcorA attenuated high glucose enhanced phosphorylation of PKCα, PKCß, PLCγ1, and the p85 subunit of PI3K. CONCLUSION: AcorA inhibits high glucose-induced extracellular matrix production via blocking NADPH oxidase activation.