The Dynamic Change in Fatty Acids during the Postharvest Process of Oolong Tea Production.

As important factors to oolong tea quality, the accumulation and dynamic change in aroma substances attracts great attention. The volatile composition of oolong tea is closely related to the precursor contents. Fatty acids (FAs) and their derivatives are basic components of oolong tea fragrance during the postharvest process. However, information about the precursors of FAs during the postharvest process of oolong tea production is rare. To investigate the transformation of fatty acids during the process of oolong tea production, gas chromatograph−flame ionization detection (GC-FID) was conducted to analyze the composition of FAs. The results show that the content of total polyunsaturated FAs initially increased and then decreased. Specifically, the contents of α-linolenic acid, linoleic acid and other representative substances decreased after the turn-over process of oolong tea production. The results of partial least squares discrimination analysis (PLS-DA) showed that five types of FAs were obviously impacted by the processing methods of oolong tea (VIP > 1.0). LOX (Lipoxygenase, EC 1.13.11.12) is considered one of the key rate-limiting enzymes of long-chain unsaturated FAs in the LOX-HPL (hydroperoxide lyase) pathway, and the mechanical wounding occurring during the postharvest process of oolong tea production greatly elevated the activity of LOX.

Combination treatment with sorafenib and wh-4 additively suppresses the proliferation of liver cancer cells.

Sorafenib is currently used to treat hepatocellular carcinoma (HCC). However, the development of chemoresistance to sorafenib is a major limitation for sorafenib-based therapy in patients with HCC. In the present study, the effect of the combination therapy of sorafenib and wh-4 on the proliferation of liver cancer cells was investigated. The results showed that sorafenib with wh-4 additively suppressed the proliferation of liver cancer cells. The colony formation of liver cancer cells decreased significantly in response to the combination treatment of sorafenib with wh-4, and it also induced the apoptosis of liver cancer cells. Western blot analysis demonstrated decreased expression of Bcl2, and increased expression of Bax in liver cancer cells treated with a combination of sorafenib and wh-4. Moreover, the migration of liver cancer cells was inhibited. The combination treatment of sorafenib with wh-4 reduced the expression levels of ABCB1 and ABCG2 which are responsible for resistance. Finally, STAT3 overexpression abolished the proliferation inhibition effect of sorafenib with wh-4 on liver cancer cells, and sorafenib and wh-4 suppressed the proliferation of liver cancer cells by STAT3 pathway. Together, these results suggest that sorafenib-wh4 combination treatment is a potential novel therapeutic approach to suppress the proliferation of liver cancer cells.

Suppression of Esophageal Cancer Stem-like Cells by SNX-2112 Is Enhanced by STAT3 Silencing.

Many studies have demonstrated that cancer stem cells (CSCs) or tumor-initiating cells (TICs) are responsible for tumor cell proliferation, chemotherapy resistance, metastasis, and relapse in various cancers. We, and others, have previously shown that the signal transducer and activator of transcription 3 (STAT3) signaling pathway is responsible for CSCs and TICs growth. Recent reports have indicated that the heat shock protein 90 (Hsp90) is also essential for the survival of CSCs and TICs. SNX-2112 is an Hsp90 inhibitor. However, it remains unclear whether proliferation of esophageal cancer stem-like cells (ECSLCs) is suppressed by SNX-2112 with knockdown of STAT3 (shSTAT3). Here, we explored the association between SNX-2112 with shSTAT3 and the suppression of ECSLCs growth. We found that the expression level of both STAT3 and p-STAT3 was higher in clinical esophageal cancer tissue than in the adjacent normal tissue, using western blot and qPCR analysis. Furthermore, differential expression analysis demonstrated that STAT3 was overexpressed in clinical specimens. We demonstrated that SNX-2112 inhibited cancer cell proliferation, decreased ABCB1 and ABCG2 gene expression levels and reduced the colony formation capacity of ECSLCs, which was enhanced by STAT3 silencing. Flow cytometry analysis revealed that the combination of SNX-2112 and shSTAT3 significantly induced apoptosis and cell cycle arrest at G2/M phase in ECSLCs. Levels of proliferation pathway proteins, including p38, c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase (ERK) which were also client proteins of Hsp90, were also reduced. In addition, SNX-2112 with shSTAT3 inhibited the proliferation of ECSLCs in vivo. Finally, STAT3 overexpression eliminated the apoptotic and antiproliferative effects of SNX-2112 on ECSLCs. Hence, these results provide a rationale for the therapeutic potential of the combination of SNX-2112 with shSTAT3 in esophageal cancer, and may indicate new targets for clinical intervention in human cancer.

Different free prostate-specific antigen to total prostate-specific antigen ratios using three detecting systems.

BACKGROUND: Prostate-specific antigen (PSA) is used as an indicative marker of a pathologic condition of the prostate, and the ratio of free PSA (fPSA) to total PSA (tPSA) helps to distinguish benign prostatic hyperplasia (BPH) from prostate cancer (PCa). In this study, we present some reversed ratios of fPSA to tPSA and analyze the possible mechanism. METHODS: Using the UniCel DxI800 Access Immunoassay System, eight reversed fPSA to tPSA ratios were obtained, and then these samples were retested with an Abbott Architect i2000 Immunoassay Analyser and Cobas e602. RESULTS: Four of the eight reversed ratios kept a ratio >1 using Abbott Architect i2000, and seven of them turned into a ratio <1 using Cobas e602. CONCLUSION: In consideration of the assay these three detecting systems apply, the possible reason of the reversed ratios can be heterophile antibodies. To get accurate reason, further study is required.

[Diagnostic capability of multidetector CT for arterioportal shunt in hepatocellular carcinoma].

OBJECTIVE: To evaluate the capability of multidetector CT (MDCT) for the diagnosis of arterioportal shunt (APS) associated with hepatocellular carcinoma (HCC). METHODS: Two hundred and eighty-two patients with HCC were examined by both enhanced thin slice MDCT scanning in early hepatic arterial phase, late hepatic arterial phase, portal venous phase and digital subtraction angiography (DSA). The criteria for diagnosis of APS: (1) Earlier enhancement or stronger opacification of main portal trunk and/or the first order branches compared with that of superior mesenteric vein or splenic vein; (2) Earlier enhancement or stronger opacification of the second order and smaller portal venous branches compared with that of main portal trunk. The presence and degree of APS demonstrated with MDCT and DSA were analysed by double blind method. RESULTS: In 282 HCC patients, 56 were complicated with APS. MDCT demonstrated central APS in 48 patients with 41 severe and 7 moderate shunt, one revealing no APS by DSA due to the giant HCC focus. Among 7 patients with light peripheral APS, two lesions were not revealed by DSA due to faint shunt and the last lesion in the patient with mixed APS was revealed both by APS and DSA. CONCLUSION: Multidetector CT was a simple, effective and noninvasive new technique for the diagnosis of arterioportal shunt associated with hepatocellular carcinoma.

Study on hepatocellular carcinoma-associated hepatic arteriovenous shunt using multidetector CT.

AIM: To investigate multidetector CT (MDCT) findings of hepatocelluar carcinoma (HCC)- associated hepatic arteriovenous shunt (HAVS) and to evaluate their clinical significance. METHODS: Thin-slice and dynamic enhancement MDCT of HAVS was performed on 56 patients with HCC. MDCT findings, including those of portal veins, hepatic veins, superior mesenteric veins, splenic veins, HCC foci, liver parenchyma without HCC foci, spleens, and thromboses in portal veins and hepatic veins, were all confirmed by digital subtract angiography and analyzed. RESULTS: MDCT demonstrated earlier enhancement of main portal trunks and/or the first order branches than that of superior mesenteric veins or splenic veins (n=31). One patient had strong early enhancement of left hepatic vein with thromboses in left hepatic vein and upper part of inferior vena cava and 1 patient had transient patchy enhancement peripheral to HCC foci in late hepatic arterial phase among them. It demonstrated stronger opacification of main portal trunks and/or the first order branches than that of superior mesenteric veins or splenic veins (n=18), and earlier enhancement of the second order and smaller branches of portal veins than that of main portal trunks (n=4), stronger opacification of the second order and smaller branches of portal veins than that of main portal trunks (n=3), with transient patchy enhancement (n=3) or wedge-shaped enhancement (n=4) peripheral to HCC foci in late hepatic arterial phase. Enhancement degree of HCC foci was all decreased. As for 49 patients with severe or moderate shunts, enhancement degree of liver parenchyma without HCC foci was increased with heterogeneous density, but enhancement degree of spleens was decreased. There were thromboses in main portal trunks and/or the first order branches in 32 patients. CONCLUSION: The main MDCT findings of HCC-associated HAVS are earlier enhancement and stronger opacification of portal veins and/or hepatic veins. Understanding of these findings will contribute to the diagnosis and prognosis of the disease and improve therapy for the patients.