Acute kidney injury in hospitalized adults with chronic kidney disease: comparing cROCK, KDIGO, and combined criteria

Ling Sun,Xue Hua Rui,Yu Wu,Lu Xi Zou 대한신장학회 2023 Kidney Research and Clinical Practice Vol.42 No.5

Background: Acute-on-chronic kidney disease (ACKD) increases the risk of progression of chronic kidney disease (CKD). This study aimed to evaluate the ability of a novel criteria of reference change value of the serum creatinine optimized criteria for acute kidney injury in CKD (cROCK) to detect ACKD patients. Methods: This was a retrospective observational study with a 3-year follow-up. All included patients with CKD stage 3 were evaluated using cROCK, Kidney Disease Improving Global Outcomes (KDIGO), and their combined criteria. The renal composite endpoints, major adverse cardiovascular events (MACEs), and all-cause mortality were recorded as clinical outcomes. Results: A total of 812 patients was enrolled. The cROCK criteria detected more ACKD events than did the KDIGO (68.0% vs. 59.5%, p < 0.001). Compared to KDIGO (−) & cROCK (−) group, ACKD patients diagnosed by cROCK had significantly higher hazard ratio [HR] for renal composite endpoints (HR, 3.591; p < 0.001), MACEs (HR, 1.748; p < 0.001), and all-cause mortality (HR, 2.985; p < 0.001). The patients in KDIGO (+) & cROCK (+) group had the lowest survival probability when considering renal composite endpoints, MACEs, and all-cause mortality (all p < 0.001). Furthermore, cROCK resulted in the largest area under the receiver operating characteristic curve (AUC) for predicting renal composite endpoints, and the combined criteria led to the largest AUC for predicting MACEs and allcause mortality. Conclusion: Compared to the KDIGO, the cROCK detected more ACKD events. Combining both cROCK and KDIGO criteria might improve the predictive ability for long-term outcomes in ACKD patients.

LncRNA CRNDE Promotes the Progression of B-cell Precursor Acute Lymphoblastic Leukemia by Targeting the miR-345-5p/CREB Axis

Weimin Wang,Feifei Wu,Ping Ma,Silin Gan,Xue Li,Li Chen,Ling Sun,Hui Sun,Zhongxing Jiang,Feng Guo 한국분자세포생물학회 2020 Molecules and cells Vol.43 No.8

The imbalance between the proliferation and apoptosis of B-cell precursors is an important contributor to the pathogenesis of B-cell precursor acute lymphoblastic leukemia (BCP-ALL), while its specific regulatory mechanism remains perplexing. This study aimed to expound the underlying mechanism of the proliferation and apoptosis of BCP-ALL cells from the perspective of non-coding RNA. In this study, long non-coding RNA colorectal neoplasia differentially expressed (LncRNA CRNDE) was upregulated in the bone marrow of BCP-ALL patients and BCP-ALL cell lines (NALM-6 and RS4;11). Functionally, LncRNA CRNDE knockdown restrained cell proliferation and boosted cell apoptosis in NALM-6 and RS4;11 cells. The subsequent investigation confirmed that LncRNA CRNDE bound to miR-345-5p and negatively regulated miR-345-5p expression. The overexpression of miR-345-5p suppressed cell proliferation and boosted cell apoptosis in NALM-6 and RS4;11 cells. Further experiments revealed that miR-345-5p downregulated cyclic AMP response element-binding protein (CREB) expression by targeting its mRNA directly. CREB overexpression reversed the effect of miR-345-5p mimic on cell proliferation and apoptosis in NALM-6 and RS4;11 cells. Finally, in vivo experiments showed that LncRNA CRNDE knockdown prolonged the survival of mice xenotransplanted with NALM-6 cells. In conclusion, LncRNA CRNDE upregulated CREB expression by suppressing miR-345-5p, thus promoting cell proliferation and reducing cell apoptosis in BCP-ALL.

Disruption of endothelial barrier function is linked with hyposecretion and lymphocytic infiltration in salivary glands of Sjögren's syndrome

Cong, Xin,Zhang, Xue-Ming,Zhang, Yan,Wei, Tai,He, Qi-Hua,Zhang, Li-Wei,Hua, Hong,Lee, Sang-Woo,Park, Kyungpyo,Yu, Guang-Yan,Wu, Li-Ling Elsevier 2018 Biochimica et biophysica acta. Molecular basis of Vol.1864 No.10

<P><B>Abstract</B></P> <P>Sjögren's syndrome (SS) is an inflammatory autoimmune disease that causes hyposecretion in salivary glands. Endothelial tight junctions (TJs) play crucial roles in salivation and barrier function of blood vessels. However, whether the alteration of endothelial TJs were involved in pathogenesis of SS was still unknown. Here, the ultrastructure and function of endothelial TJs in submandibular glands (SMGs) were detected by transmission electron microscopy and in vivo paracellular permeability assay in different aged NOD mouse model for SS. CFSE-labeled lymphocytes were injected into tail vein to trace the infiltration, while claudin-5 expression and distribution were detected by immunofluorescence, qRT-PCR, and western blot. Results showed that the stimulated salivary flow rate was gradually decreased and lymphocytic infiltration was found as age increased in 12- and 21-week-old NOD mice, but not 7-week-old NOD mice. Blood vessels were dilated, while endothelial TJ width and paracellular tracer transport were increased in 12-week-old NOD mice. Moreover, the injected CFSE-labeled lymphocytes were observed in SMGs of 12-week-old NOD mice. Claudin-5 level was increased and relocalized from the apical portion of neighboring endothelial cells to lateral membranes and cytoplasm in 12-week-old NOD mice. Additionally, the alteration of claudin-5 expression and distribution was further confirmed in labial salivary glands and bilateral parotid glands from SS patients. In cultured human microvessel endothelial cell line (HMEC-1), IFN-γ stimulation significantly increased claudin-5 expression. Taken together, we identified that the endothelial TJ barrier was disrupted and contributed to the development of salivary hyposecretion and lymphocytic infiltration in SS.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Endothelial tight junction barrier is disrupted in hyposecretory submandibular glands from Sjögren's syndrome mouse model </LI> <LI> The disrupted salivary endothelial barrier is linked with lymphocytic infiltration in Sjögren's syndrome mouse model </LI> <LI> The redistribution of claudin-5 is responsible for disrupted endothelial barrier in salivary glands from Sjögren's syndrome </LI> </UL> </P>

Molecular Mechanism of Plant Growth Promotion and Induced Systemic Resistance to Tobacco Mosaic Virus by Bacillus spp.

Shuai Wang,Hui Jun Wu,Jun Qing Qiao,Ling Li Ma,Jun Liu,Yan Fei Xia,Xue Wen Gao 한국미생물 · 생명공학회 2009 Journal of microbiology and biotechnology Vol.19 No.10

Colorectal Cancer Mortality Characteristics and Predictions in China, 1991-2011

Fang, Jia-Ying,Dong, Hong-Li,Sang, Xue-Jin,Xie, Bin,Wu, Ku-Sheng,Du, Pei-Ling,Xu, Zhen-Xi,Jia, Xiao-Yue,Lin, Kun Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.17

Background: To identify the epidemiological characteristics of colorectal cancer mortality in China during the period of 1991-2011, and forecast the future five-year trend. Materials and Methods: Mortality data for colorectal cancer in China from 1991 to 2011 was used to describe epidemiological characteristics in terms of age group, gender, and rural/urban residence. Trend surface analysis was performed to analyze the geographical distribution of colorectal cancer. Four models including curve estimation, time series modeling, gray modeling and joinpoint regression were applied to forecast the trends for the future five years. Results: Since 1991 the colorectal cancer mortality rate increased yearly, and our results showed that the trend would continue to increase in the ensuing 5 years. The mortality rate in males was higher than that of females and the rate in urban areas was higher than in rural areas. The mortality rate was relatively low for individuals less than 60 years of age, but increased dramatically afterwards. People living in the northeastern China provinces or in eastern China had a higher mortality rate for colorectal cancer than those living in middle or western China provinces. Conclusions: The steadily increasing mortality of colorectal cancer in China will become a substantial public health burden in the foreseeable future. For this increasing trend to be controlled, further efforts should concentrate on educating the general public to increase prevention and early detection by screening. More effective prevention and management strategies are needed in higher mortality areas (Eastern parts of China) and high-risk populations (60+ years old).

Caryophyllene oxide inhibits migration and invasion of endometrial cancer cells

Chi-Chang CHANG,Hsia-Fen HSU,Jing-Mei WU,Xue-Hua LING,Jer-Yiing HOUNG 한국생물공학회 2016 한국생물공학회 학술대회 Vol.2016 No.4

4-Hydroxynonenal Promotes Growth and Angiogenesis of Breast Cancer Cells through HIF-1α Stabilization

Li, Yao-Ping,Tian, Fu-Guo,Shi, Peng-Cheng,Guo, Ling-Yun,Wu, Hai-Ming,Chen, Run-Qi,Xue, Jin-Ming Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.23

4-Hydroxynonenal (4-HNE) is a stable end product of lipid peroxidation, which has been shown to play an important role in cell signal transduction, while increasing cell growth and differentiation. 4-HNE could inhibit phosphatase and tensin homolog (PTEN) activity in hepatocytes and increased levels have been found in human invasive breast cancer. Here we report that 4-HNE increased the cell growth of breast cancer cells as revealed by colony formation assay. Moreover, vascular endothelial growth factor (VEGF) expression was elevated, while protein levels of hypoxia inducible factor 1 alpha (HIF-$1{\alpha}$) were up-regulated. Sirtuin-3 (SIRT3), a major mitochondria NAD+-dependent deacetylase, is reported to destabilize HIF-$1{\alpha}$. Here, 4-HNE could inhibit the deacetylase activity of SIRT3 by thiol-specific modification. We further demonstrated that the regulation by 4-HNE of levels of HIF-$1{\alpha}$ and VEGF depends on SIRT3. Consistent with this, 4-HNE could not increase the cell growth in SIRT3 knockdown breast cancer cells. Additionally, 4-HNE promoted angiogenesis and invasion of breast cancer cells in a SIRT3-dependent manner. In conclusion, we propose that 4-HNE promotes growth, invasion and angiogenesis of breast cancer cells through the SIRT3-HIF-$1{\alpha}$-VEGF axis.

Ferric Reductase Activity of the ArsH Protein from Acidithiobacillus ferrooxidans

( Mo Hong Yu ),( Qian Chen ),( Juan Du ),( Lin Tang ),( Fang Qin ),( Bo Miao ),( Xue Ling Wu ),( Jia Zeng ) 한국미생물 · 생명공학회 2011 Journal of microbiology and biotechnology Vol.21 No.5

The arsH gene is one of the arsenic resistance system in bacteria and eukaryotes. The ArsH protein was annotated as a NADPH-dependent flavin mononucleotide (FMN) reductase with unknown biological function. Here we report for the first time that the ArsH protein showed high ferric reductase activity. Glu104 was an essential residue for maintaining the stability of the FMN cofactor. The ArsH protein may perform an important role for cytosolic ferric iron assimilation in vivo.

Betulin Targets Lipin1/2-Meidated P2X7 Receptor as a Therapeutic Approach to Attenuate Lipid Accumulation and Metaflammation

( Jia-yi Dou ),( Yu-chen Jiang ),( Zhong-he Hu ),( Kun-chen Yao ),( Ming-hui Yuan ),( Xiao-xue Bao ),( Mei-jie Zhou ),( Yue Liu ),( Zhao-xu Li ),( Li-hua Lian ),( Ji-xing Nan ),( Yan-ling Wu ) 한국응용약물학회 2022 Biomolecules & Therapeutics(구 응용약물학회지) Vol.30 No.3

The present study focused on the potential mechanism of betulin (BT), a pentacyclic triterpenoid isolated from the bark of white birch (Betula pubescens), against chronic alcohol-induced lipid accumulation and metaflammation. AML-12 and RAW 264.7 cells were administered ethanol (EtOH), lipopolysaccharide (LPS) or BT. Male C57BL/6 mice were fed Lieber-DeCarli liquid diets containing 5% EtOH for 4 weeks, followed by single EtOH gavage on the last day and simultaneous treatment with BT (20 or 50 mg/kg) by oral gavage once per day. In vitro, MTT showed that 0-25 mM EtOH and 0-25 μM BT had no toxic effect on AML-12 cells. BT could regulate sterolregulatory-element-binding protein 1 (SREBP1), lipin1/2, P2X7 receptor (P2X7r) and NOD-like receptor family, pyrin domains-containing protein 3 (NLRP3) expressions again EtOH-stimulation. Oil Red O staining also indicated that BT significantly reduced lipid accumulation in EtOH-stimulated AML-12 cells. Lipin1/2 deficiency indicated that BT might mediate lipin1/2 to regulate SREBP1 and P2X7r expression and further alleviate lipid accumulation and inflammation. In vivo, BT significantly alleviated histopathological changes, reduced serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and triglyceride (TG) levels, and regulated lipin1/2, SREBP1, peroxisome proliferator activated receptor α/γ (PPARα/γ) and PGC-1α expression compared with the EtOH group. BT reduced the secretion of inflammatory factors and blocked the P2X7r-NLRP3 signaling pathway. Collectively, BT attenuated lipid accumulation and metaflammation by regulating the lipin1/2-mediated P2X7r signaling pathway.

Risk of venous thromboembolism in Chinese pregnant women: Hong Kong venous thromboembolism study

Duo Huang,Emmanuel Wong,Ming-Liang Zuo,Pak-Hei Chan,Wen-Sheng Yue,Hou-Xiang Hu,Ling Chen,Li-Xue Yin,Xin-Wu Cui,Ming-Xiang Wu,Xi Su,Chung-Wah Siu,Jo-Jo Hai 대한혈액학회 2019 Blood Research Vol.54 No.3

BackgroundPrevious Caucasian studies have described venous thromboembolism in pregnancy; however, little is known about its incidence during pregnancy and early postpartum peri-od in the Chinese population. We investigated the risk of venous thromboembolism in a “real-world” cohort of pregnant Chinese women with no prior history of venous thromboembolism.MethodsIn this observational study, 15,325 pregnancies were identified in 14,162 Chinese women at Queen Mary Hospital, Hong Kong between January 2004 and September 2016. Demographic data, obstetric information, and laboratory and imaging data were retrieved and reviewed.ResultsThe mean age at pregnancy was 32.4±5.3 years, and the median age was 33 years (interquartile range, 29‒36 yr). Pre-existing or newly diagnosed diabetes mellitus was present in 627 women (4.1%); 359 (0.7%) women had pre-existing or newly detected hypertension. There was a small number of women with pre-existing heart disease and/or rheumatic conditions. Most deliveries (86.0%) were normal vaginal; the remaining were Cesarean section 2,146 (14.0%). The incidence of venous thromboembolism was 0.4 per 1,000 pregnancies, of which 83.3% were deep vein thrombosis and 16.7% were pul-monary embolism. In contrast to previous studies, 66.7% of venous thrombosis occurred in the first trimester.ConclusionChinese women had a substantially lower risk of venous thromboembolism during preg-nancy and the postpartum period compared to that of Caucasians. The occurrence of pregnancy-related venous thromboembolism was largely confined to the early preg-nancy period, probably related to the adoption of thromboprophylaxis, a lower rate of Cesarean section, and early mobilization.