Plant resistance against whitefly and its engineering.

Plants face constant threats from insect herbivores, which limit plant distribution and abundance in nature and crop productivity in agricultural ecosystems. In recent decades, the whitefly Bemisia tabaci, a group of phloem-feeding insects, has emerged as pests of global significance. In this article, we summarize current knowledge on plant defenses against whitefly and approaches to engineer plant resistance to whitefly. Physically, plants deploy trichome and acylsugar-based strategies to restrain nutrient extraction by whitefly. Chemically, toxic secondary metabolites such as terpenoids confer resistance against whitefly in plants. Moreover, the jasmonate (JA) signaling pathway seems to be the major regulator of whitefly resistance in many plants. We next review advances in interfering with whitefly-plant interface by engineering of plant resistance using conventional and biotechnology-based breeding. These breeding programs have yielded many plant lines with high resistance against whitefly, which hold promises for whitefly control in the field. Finally, we conclude with an outlook on several issues of particular relevance to the nature and engineering of plant resistance against whitefly.

HCV inhibits M2a, M2b and M2c macrophage polarization via HCV core protein engagement with Toll-like receptor 2.

Hepatitis C virus (HCV) establishes a persistent infection in most patients, eventually leading to chronic hepatitis C (CHC), cirrhosis and hepatocellular carcinoma. Our previous study revealed that HCV core protein (HCVc) inhibited the differentiation of monocytes into M1 and M2 macrophages. However, it remains unclear as to whether HCVc affects the polarization of M2 macrophages, and if this effect promotes the progression of chronic disease. In the present study, peripheral blood mononuclear cells (PBMCs) from patients with CHC and healthy controls (HCs) were isolated, purified and polarized to M2a, M2b and M2c macrophages. Phenotypic expression, cytokine secretion and gene expression were analyzed using flow cytometry, ELISA and reverse transcription-quantitative polymerase chain reaction, respectively. Monocytes from HCs were cultured with HCVc to study the effect of HCVc on macrophage polarization. Plasma alanine transaminase and HCV-RNA levels were significantly higher, and albumin levels were significantly lower in the CHC group than those in the control group (P<0.05). M2a macrophages polarized from monocytes of patients with CHC expressed lower levels of CD209, IL-1 receptor antagonist (IL-1RA) and Fizz1 compared with those from HCs. M2b macrophages expressed lower levels of CD86 and TNF-α, and M2c macrophages expressed lower levels of CD163, TGF-ß and sphingosine kinase 1 (SPHK1) in the CHC group compared with HCs (P<0.05). HCVc inhibited the expression levels of CD209, IL-1RA and Fizz1 in M2a macrophages; CD86 and TNF-α in M2b macrophages; and CD163, TGF-ß and SPHK1 in M2c macrophages (P<0.05). HCVc significantly suppressed phagocytosis of all subtypes (P<0.05); however, this inhibition was restored by an anti-Toll-like receptor (TLR)2 antibody (P<0.05). In conclusion, HCVc inhibited monocyte-derived M2a, M2b and M2c subtype differentiation via the TLR2 signaling pathway, resulting in macrophages exhibiting reduced phagocytosis in patients with CHC. This may contribute to persistent HCV infection, thus suggesting that the blockade of HCVc may be a new therapeutic approach for the treatment of HCV infection.

Prognostic performance of clinical indices and model scorings for acute-on-chronic liver failure: A study of 164 patients.

The present study aimed to analyze the prognostic factors of acute-on-chronic liver failure (ACLF), with the perspective of an improved selection of optimal therapeutic schemes. A retrospective analysis was used to study 164 patients with ACLF hospitalized between 2010 and 2014 in a single center. Patients were divided into favorable and unfavorable groups, according to the treatment outcomes. General characteristics and clinical manifestations were analyzed to determine whether they would affect the prognosis of the patients with ACLF, with a particular focus on the scoring systems Child-Pugh, model for end-stage liver disease (MELD), MELD with incorporation of sodium (MELD-Na), MELD and serum sodium ratio (MESO) and integrated MELD (iMELD). Hepatitis B virus infection was the predominant cause of ACLF, accounting for 88 cases (53.7%). Age, prothrombin time, thrombin time, international normalized ratio (INR), prothrombin activity, serum sodium, albumin, total bilirubin, serum creatinine, platelets, fasting blood sugar, infections, hepatic encephalopathy, hepatorenal syndrome (HRS), and electrolyte disorder were revealed to be associated with prognosis. Age, serum sodium, INR, HRS, and infection were independent prognostic risk factors, as determined by multivariate analysis. Child-Pugh, MELD, MELD-Na, MESO and iMELD scoring systems all demonstrated adequate predictive values, with MELD-Na as the most effective scoring system. In conclusion, age, hyponatremia, INR, HRS and bacterial or fungal infections were reported to be independent prognostic risk factors for ACLF. Among the various liver function scoring systems, MELD-Na was the most accurate in predicting the prognosis of ACLF.

MicroRNA-381 suppresses cell growth and invasion by targeting the liver receptor homolog-1 in hepatocellular carcinoma.

MicroRNAs (miRs) have emerged as prospective tools for human cancer therapy, including hepatocellular carcinoma (HCC) therapy. Previous studies have suggested that miR-381 functions as oncogenic or tumor-suppressive miRs in other cancer types. However, the role of miR-381 in HCC remains unknown. The present study investigated the expression and functional role of miR-381 in HCC. miR-381 expression was significantly decreased in HCC tissues and cell lines. miR-381 overexpression significantly inhibited HCC cell proliferation and colony formation, induced G0/G1 cell cycle arrest and suppressed cell invasion. Conversely, suppression of miR-381 showed the opposite effect in HCC cells. Bioinformatics analysis and dual-luciferase reporter assay results showed that miR-381 directly targeted the 3'-untranslated region of liver receptor homolog-1 (LRH-1), and quantitative polymerase chain reaction and western blot analysis results showed that miR-381 negatively modulated LRH-1 expression. Data elucidated that miR-381 directly regulated HCC cell growth and invasion, as well as the Wnt signaling pathways, by targeting LRH-1. Clinical tissue detection data revealed an inverse correlation between miR-381 and LRH-1 expression in HCC tissues, further indicating the functional significance of miR-381-LRH-1 in regulating HCC tumorigenesis. The present study indicates that miR-381 may be a novel tumor suppressor that blocks HCC growth and invasion by targeting LRH-1. The results present novel insights into understanding the molecular mechanism underlying HCC tumorigenesis and provide a future direction to the development of therapeutic interventions for HCC.

Ulinastatin suppresses endoplasmic reticulum stress and apoptosis in the hippocampus of rats with acute paraquat poisoning.

Lung injury is the main manifestation of paraquat poisoning. Few studies have addressed brain damage after paraquat poisoning. Ulinastatin is a protease inhibitor that can effectively stabilize lysosomal membranes, prevent cell damage, and reduce the production of free radicals. This study assumed that ulinastatin would exert these effects on brain tissues that had been poisoned with paraquat. Rat models of paraquat poisoning were intraperitoneally injected with ulinastatin. Simultaneously, rats in the control group were administered normal saline. Hematoxylin-eosin staining showed that most hippocampal cells were contracted and nucleoli had disappeared in the paraquat group. Fewer cells in the hippocampus were concentrated and nucleoli had disappeared in the ulinastatin group. Western blot assay showed that expressions of GRP78 and cleaved-caspase-3 were significantly lower in the ulinastatin group than in the paraquat group. Immunohistochemical findings showed that CHOP immunoreactivity was significantly lower in the ulinastatin group than in the paraquat group. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining showed that the number of apoptotic cells was reduced in the paraquat and ulinastatin groups. These data confirmed that endoplasmic reticular stress can be induced by acute paraquat poisoning. Ulinastatin can effectively inhibit this stress as well as cell apoptosis, thereby exerting a neuroprotective effect.

[Clinical significance of dynamic monitoring of procalcitonin in guiding the use of antibiotics in patients with sepsis in ICU].

OBJECTIVE: To investigate the significance of dynamic monitoring of procalcitonin (PCT) in guiding the use of antibiotics for treating patients with sepsis in intensive care unit (ICU). METHODS: Eighty-two patients with sepsis from January 2012 to June 2013 hospitalized in ICU of First Hospital of Jilin University were enrolled, and they were randomly divided into regular antibiotic therapy group (RAT group, n=40) and PCT monitoring in guiding the use of antibiotics group (PCT group, n=42). Patients in RAT group were treated according to principle of antibiotics usage, while in PCT group patients' PCT value was observed everyday. When no active symptoms of infection were shown, and acute physiology and chronic health evaluation II (APACHEII) scores declined, PCT value decreased over 90% or PCT value lower than 0.25 µg/L time point were selected as drug withdrawal indication. The general status of the patient, antimicrobial drug use time, and prognosis were compared between the two groups, and Kaplan-Meier method was used for survival curve analysis. Variance analysis was used for repeating measurement to observe dynamic serum PCT level of the two groups of patients for survival and death during 7 days. RESULTS: Mann-Whitney U test or χ(2) test showed that there were no statistical significance in age, gender, APACHEII score, blood culture positive rate, sputum culture positive rate, cardiac insufficiency, renal failure, respiratory failure, and ventilator and hemofiltration usage (all P>0.05). Log Rank test results showed that the time of antimicrobial drug usage was significantly reduced in PCT group than that in RAT group [days: 8.1±0.3, 95% confidence interval (95%CI 8.3-9.7) vs. 9.3±0.3 (95%CI 8.7-10.1), P=0.013]. Kaplan-Meier univariate survival curves showed that the speed of curve declination in PCT group was faster significantly than that in RAT group, suggesting that the time of using antimicrobial drug was shortened. There was no significant difference in length of hospital stay, ICU stay time, number of death in 28 days, number of cases of recurrence in 28 days and clinical cure rate between two groups (all P>0.05). PCT level in non-survivors in both groups was significantly higher than that in the survivors, exceeding more than 10 µg/L in the early and late stages of treatment. CONCLUSIONS: Dynamic monitoring of PCT can effectively reduce antimicrobial drug use in ICU patients with sepsis, but there is no significant difference in patients' prognosis.