Search

Background Patients with liver cirrhosis complicated by gastroesophageal variceal and rupture hemorrhage have a certain probability of rebleeding events after endoscopic treatment, and the bleeding volume of rebleeding events is greater with higher risk, which seriously affects the survival rates of patients. Objective To investigate the independent risk factors of rebleeding events within 3 years after endoscopic treatment in cirrhotic patients with gastroesophageal variceal hemorrhage, construct a nomogram risk prediction model and validate it internally. Methods Four hundred and three patients who underwent endoscopic treatment for liver cirrhosis associated gastroesophageal varices at the Tangdu Hospital and Xijing Hospital, Air Force Medical University from 2011-2022 were retrospectively collected and divided into the rebleeding group (n=252) and control group (n=151) based on the presence of rebleeding within 3 years. The general data and auxiliary examination results of the patients between both groups were compared, and the statistically significant factors were included in the multivariate Logistic regression analysis to analyze the independent risk factors. These data were then input into the R language software to construct a nomogram risk prediction model by using a specific program package. Results Multivariate Logistic regression analysis showed that smoking〔OR=2.499, 95%CI (1.232, 5.066), P=0.011〕, portal vein internal diameter〔OR=1.047, 95%CI (1.028, 1.066), P

Phosphodiesterase 2 (PDE2A) modulates the levels of cAMP/cGMP and was recently found to be involved in mitochondria function regulation, closely related to multiple types of tumor progression. This study aimed to estimate the prognostic significance and biological effects of PDE2A on hepatocellular carcinoma (HCC). We comprehensively analyzed the PDE2A mRNA expression in HCC based on The Cancer Genome Atlas (TCGA) database and investigated the effects of PDE2A on the proliferation and metastatic capacity of HCC cells. PDE2A was downregulated in 25 cancer types, including HCC. Lower PDE2A expression was a protective factor in HCC and was negatively associated with serum AFP levels, tumor status, vascular invasion, histologic grade, and pathologic stage of HCC. Moreover, tumors with low PDE2A expression displayed a decreased immune function. Then, the ROC curve was used to assess the diagnostic ability of PDE2A in HCC (AUC = 0.823 in TCGA and AUC = 0.901 in GSE76427). Patients with low PDE2A expression exhibited worse outcomes compared with those with high PDE2A expression. Additionally, GO functional annotations demonstrated the involvement of PDE2A in the ECM organization, systems development, and ERK-related pathways, indicating that PDE2A might regulate HCC growth and metastasis. The in vitro experiments confirmed that overexpression of PDE2A inhibited proliferation, colony formation, migration, and invasion in two HCC cell lines (HLF and SNU-368), while inhibition of PDE2A has the opposite results. The mechanism of PDE2A's effect on HCC cells is attributed to the change of mitochondrial morphology and ATP content. These data demonstrated that PDE2A closely participated in the regulation of HCC proliferation and metastasis and can be used as a predictive marker candidate and a potential therapeutic target for HCC. [ABSTRACT FROM AUTHOR]

Non-invasive micro-test techniques (NMT) were used to analyze NaCl-altered flux profiles of K+, Na+, and H+ in roots and effects of NaHS (a H2S donor) on root ion fluxes in two contrasting poplar species, Populus euphratica (salt-resistant) and Populus popularis (salt-sensitive). Both poplar species displayed a net K+ efflux after exposure to salt shock (100 mM NaCl), as well as after short-term (24 h), and long-term (LT) (5 days) saline treatment (50 mM NaCl, referred to as salt stress). NaHS (50 μM) restricted NaCl-induced K+ efflux in roots irrespective of the duration of salt exposure, but K+ efflux was not pronounced in data collected from the LT salt stress treatment of P. euphratica. The NaCl-induced K+ efflux was inhibited by a K+ channel blocker, tetraethylammonium chloride (TEA) in P. popularis root samples, but K+ loss increased with a specific inhibitor of plasma membrane (PM) H+-ATPase, sodium orthovanadate, in both poplar species under LT salt stress and NaHS treatment. This indicates that NaCl-induced K+ loss was through depolarization-activated K+ channels. NaHS caused increased Na+ efflux and a corresponding increase in H+ influx for poplar roots subjected to both the short- and LT salt stress. The NaHS-enhanced H+ influx was not significant in P. euphratica samples subjected to short term salt stress. Both sodium orthovanadate and amiloride (a Na+/H+ antiporter inhibitor) effectively inhibited the NaHS-augmented Na+ efflux, indicating that the H2S-enhanced Na+ efflux was due to active Na+ exclusion across the PM. We therefore conclude that the beneficial effects of H2S probably arise from upward regulation of the Na+/H+ antiport system (H+ pumps and Na+/H+ antiporters), which promote exchange of Na+ with H+ across the PM and simultaneously restricted the channel-mediated K+ loss that activated by membrane depolarization. [ABSTRACT FROM AUTHOR]

Acer truncatum seed coat is generally abandoned as waste during the process of manufacturing seed oil due to a lack of knowledge of the phytochemical composition of this byproduct. It is well known that brown-colored seed coat is rich in polyphenols; therefore, we investigated the bioactive phenolic composition of A. truncatum seed coat in this study. To obtain an extract containing most bioactive phenolic compounds, extractions in six solutions (water, 40% ethanol, 70% ethanol, 100% ethanol, 70% acetone, and 100% acetone) were compared for their yields, phenolic contents, and antioxidant activities. The 70% ethanol extract, which had the highest yield at 76.38 g extract/100 g dry matter, showed the highest levels of total phenols, total flavonoids, total tannins, and condensed tannins, as well as the highest DPPH and ABTS + scavenging activities. UPLC-QTOF-MS analyses resulted in identification of 13 phenolic compounds in the 70% ethanol extract, among which five compounds, gentisic acid, naringenin, epicatechin, procyanidin tetramer, and procyanidin pentamer, were identified for the first time in A . truncatum . Five flavonoids and four procyanidin oligomers were the dominant phenolic components, comprising 63.27% and 31.02% of the 13 phenolic compounds, respectively. Correlation analyses revealed that flavonoids and tannins were the major factors responsible for the high antioxidant activities, suggesting that these two components of A. truncatum seed coat could be developed as alternative antioxidants. This is the first known report on the phenolic composition of seed coats in the genus Acer . [ABSTRACT FROM AUTHOR]

Non-invasive micro-test techniques (NMT) were used to analyze NaCl-altered flux profiles of K + , Na + , and H + in roots and effects of NaHS (a H 2 S donor) on root ion fluxes in two contrasting poplar species, Populus euphratica (salt-resistant) and Populus popularis (salt-sensitive). Both poplar species displayed a net K + efflux after exposure to salt shock (100 mM NaCl), as well as after short-term (24 h), and long-term (LT) (5 days) saline treatment (50 mM NaCl, referred to as salt stress). NaHS (50 μM) restricted NaCl-induced K + efflux in roots irrespective of the duration of salt exposure, but K + efflux was not pronounced in data collected from the LT salt stress treatment of P. euphratica . The NaCl-induced K + efflux was inhibited by a K + channel blocker, tetraethylammonium chloride (TEA) in P. popularis root samples, but K + loss increased with a specific inhibitor of plasma membrane (PM) H + -ATPase, sodium orthovanadate, in both poplar species under LT salt stress and NaHS treatment. This indicates that NaCl-induced K + loss was through depolarization-activated K + channels. NaHS caused increased Na + efflux and a corresponding increase in H + influx for poplar roots subjected to both the short- and LT salt stress. The NaHS-enhanced H + influx was not significant in P. euphratica samples subjected to short term salt stress. Both sodium orthovanadate and amiloride (a Na + /H + antiporter inhibitor) effectively inhibited the NaHS-augmented Na + efflux, indicating that the H 2 S-enhanced Na + efflux was due to active Na + exclusion across the PM. We therefore conclude that the beneficial effects of H 2 S probably arise from upward regulation of the Na + /H + antiport system (H + pumps and Na + /H + antiporters), which promote exchange of Na + with H + across the PM and simultaneously restricted the channel-mediated K + loss that activated by membrane depolarization.