Field Control Effect and Initial Mechanism: A Study of Isobavachalcone against Blister Blight Disease.

Blister blight (BB) disease is caused by the obligate biotrophic fungal pathogen Exobasidium vexans Massee and seriously affects the yield and quality of Camellia sinensis. The use of chemical pesticides on tea leaves substantially increases the toxic risks of tea consumption. Botanic fungicide isobavachalcone (IBC) has the potential to control fungal diseases on many crops but has not been used on tea plants. In this study, the field control effects of IBC were evaluated by comparison and in combination with natural elicitor chitosan oligosaccharides (COSs) and the chemical pesticide pyraclostrobin (Py), and the preliminary action mode of IBC was also investigated. The bioassay results for IBC or its combination with COSs showed a remarkable control effect against BB (61.72% and 70.46%). IBC, like COSs, could improve the disease resistance of tea plants by enhancing the activity of tea-plant-related defense enzymes, including polyphenol oxidase (PPO), catalase (CAT), phenylalanine aminolase (PAL), peroxidase (POD), superoxide dismutase (SOD), ß-1,3-glucanase (Glu), and chitinase enzymes. The fungal community structure and diversity of the diseased tea leaves were examined using Illumina MiSeq sequencing of the internal transcribed spacer (ITS) region of the ribosomal rDNA genes. It was obvious that IBC could significantly alter the species' richness and the diversity of the fungal community in affected plant sites. This study broadens the application range of IBC and provides an important strategy for the control of BB disease.

The Relationship Between the Neutrophil to Lymphocyte Ratio, The Platelet to Lymphocyte Ratio, and Cardiac Syndrome X.

Objective: This study aims to investigate the relationship between the neutrophil to lymphocyte ratio (NLR), the platelet to lymphocyte ratio (PLR), and cardiac syndrome X (CSX). Methods: A total of 102 patients with CSX who were hospitalized in the Cardiology Department of our hospital from December 2018 to December 2020 were enrolled in the CSX group, and 102 subjects who underwent physical examinations during the same period were included in the control group. An automatic blood cell analyzer was adopted to detect the neutrophil count (NC), lymphocyte count (LC), and number of platelets (PLT) in the whole blood of the subjects in both groups, and the NLR and PLR were calculated. Electrocardiography was conducted on the subjects in both groups to detect whether any abnormality existed in the ST segment. The receiver operating curve (ROC) was used to evaluate the diagnostic value of each indicator of CSX, and multivariate logistic regression analysis was adopted for the analysis of the influencing factors. Results: No significant differences existed in age, gender, smoking history, or family history of diabetes mellitus, hypertension, and tumors between the two groups (p > 0.05). When compared with the control group, the NC, PLT, NLR, PLR, and rate of abnormality of the ST segment on the electrocardiogram were significantly higher, and the LC was significantly lower in the CSX group (p < 0.05). Multivariate logistic regression analysis showed that the ST-segment abnormality (3.95 [2.10~7.41]; NLR > 2.21, 3.46 [1.87~6.39]; and PLR > 119.77, 3.66 [1.99~6.73]) was a correlated risk factor for the occurrence of CSX (p < 0.05). Conclusion: Both the NLR and PLR in patients with CSX were significantly elevated, and both have a certain predictive value for the occurrence of CSX and are expected to be effective biomarkers for CSX.

Transcriptome Analysis on the Mechanism of Ethylicin Inhibiting Pseudomonas syringae pv. actinidiae on Kiwifruit.

Bacterial canker disease caused by Pseudomonas syringae pv. actinidiae (Psa) is a devastating disease of kiwifruit, which is severely limiting the development of the kiwifruit industry. Ethylicin is a broad-spectrum plant biomimetic fungicide. However, its application in the control of kiwifruit bacterial canker is rarely reported, and the mechanism of ethylicin on Psa remains unknown. In this study, we investigated the effect of ethylicin on Psa in vitro and in vivo and found that ethylicin can inhibit the growth of Psa and prevent the cankering in the plant stem. Mechanism investigation indicated that ethylicin acted by limiting the movement of Psa, destroying the cell membrane of Psa, and inhibiting the formation of Psa biofilm. In addition, it was also found through transcriptomics research that ethylicin can up-regulate the expression of genes related to protein export and biofilm formation-Pseudomonas aeruginosa and down-regulate the expression of genes related to flagellar assembly in Psa. This study concluded that ethylicin can effectively inhibit Psa growth, and it could help to gain a better understanding of the mechanisms of ethylicin inhibiting Psa and provide practical data for the application of ethylicin as a highly potent agent for controlling the bacterial canker disease of kiwifruit.

Increased Serum CA125 and Brain-Derived Neurotrophic Factor (BDNF) Levels on Acute Myocardial Infarction: A Predictor for Acute Heart Failure.

BACKGROUND This study was conducted to see whether increased values of serum CA125 and BDNF (brain-derived neurotrophic factor) on acute myocardial infarction (AMI) act as predictor for acute heart failure (AHF). MATERIAL AND METHODS Seventy-eight patients with clinically diagnosed cardiac function II-IV; and AHF were considered as the study group of this retrospective study and patients who had cardiac function I (without AHF) were considered the control group (n=82). The values of CA125 and BDNF were measured using enzyme-linked immunosorbent assay (ELISA) for developing the correlation with the Killip classification, and the diagnostic value of AHF. RESULTS Statistically insignificant difference was noticed between baseline information e.g., blood pressure or smoking status of participants in study group and control group (P>0.05). The higher values of CA125 (5.68±1.8 U/mL or BDNF (19.48±5.3 pg/mL) in the study group had advantage over the control after independent sample t-test (P<0.001). A positive correlation was observed between values of the test substances and Killip classifications (I-IV) of cardiac functioning was observed (r=0.745, P<0.001; Spearman's rank correlation coefficient). The sensitivity and specificity of area under the curve (AUC) combined with serum CA125 and BDNF levels in the diagnosis of AHF was 91.02% and 81.63%, respectively. CONCLUSIONS Increased serum level of the test substances indicates severity of AHF-leading AMI. Thus, monitoring is needed to avoid risk of AHF.

[Cardiac protection from myocardial ischemic postconditioning and remote postconditioning during myocardial ischemia/reperfusion injury in rabbits].

OBJECTIVE: To observe whether there are some differences between myocardial postconditioning and remote postconditioning, and whether there is additional cardiac protection when they are used combined during myocardial ischemia/reperfusion injury in rabbits. METHODS: Thirty healthy New Zealand rabbits which were randomly divided into 5 groups (n = 5): ischemic control group (CON), sham operation group (Sham), myocardial postconditioning group (MPostC), remote postconditioning group (RPostC), myocardial postconditioning plus remote postconditioning group (MPostC + RPostC). Acute myocardial infarction was induced by 45 minutes occlusion on left circumflex coronary artery (LCX) and 2 hours reperfusion in all anesthetized open-chest rabbits except the Sham, the coronary occlusion and reperfusion were determined by changes of ECG and cardiac color. Skeletal muscle ischemia model was induced by extrinsic iliac arteries occlusion and reperfusion with artery clamps. The condition that the extrinsic iliac arteries were occluded or reperfused could be tested by according to the distal arterial pulse. Plasma creatine kinase (CPK) activity and lactate dehydrogenase (LDH) activity were measured at baseline, the end of ischemia, after 1 hour and 2 hours of reperfusion respectively. The extent of myocardial infarction was assessed by triphenyltetrazolium (TTC) staining and measured by area ratio of AN/AAR. RESULTS: Compared with the Con, myocardial infarct size was significantly reduced in MPostC and RpostC group (P < 0.05). But there was no significant difference between MPostC and RPostC group. Combined MPostC and RPostC markedly enhanced myocardial protection (P < 0.05). The trend of CPK and LDH release was similar to the trend of myocardial infarct size. CONCLUSION: Both MPostC and RPostC induced cardiac protection. There was no significant difference between MPostC and RPostC. Combined MPostC and RPostC induced markedly additive effect on myocardial protection.