Detection of Reactive Oxygen Species in Plant Root Immunity.

Reactive oxygen species (ROS) production is a key early defense mechanism in plants when exposed to biotic stress. Upon recognition of conserved microbe-associated molecular patterns (MAMPs) from pathogens by plant receptors, nicotinamide adenine dinucleotide phosphate (NADPH) oxidases in the plasma membrane are activated to produce hydrogen peroxide (H2O2). This, in turn, regulates multiple signaling pathways to trigger immunity and suppress pathogen infection. Monitoring the ROS burst in plant leaves can be done within minutes of MAMPs treatment. However, there is limited research on the quantification of ROS production in plant root tissues during the activation of plant immunity. In this study, we introduce a rapid, accessible, and straightforward technique for measuring MAMPs-triggered ROS bursts in the roots of the model legume Medicago truncatula. This method will facilitate the investigation of plant root responses to biotic and abiotic stresses.

MYB30 integrates light signals with antioxidant biosynthesis to regulate plant responses during postsubmergence recovery.

Submergence is an abiotic stress that limits agricultural production world-wide. Plants sense oxygen levels during submergence and postsubmergence reoxygenation and modulate their responses. Increasing evidence suggests that completely submerged plants are often exposed to low-light stress, owing to the depth and turbidity of the surrounding water; however, how light availability affects submergence tolerance remains largely unknown. Here, we showed that Arabidopsis thaliana MYB DOMAIN PROTEIN30 (MYB30) is an important transcription factor that integrates light signaling and postsubmergence stress responses. MYB DOMAIN PROTEIN30 protein abundance decreased upon submergence and accumulated during reoxygenation. Under submergence conditions, CONSTITUTIVE PHOTOMORPHOGENIC1 (COP1), a central regulator of light signaling, caused the ubiquitination and degradation of MYB30. In response to desubmergence, however, light-induced MYB30 interacted with MYC2, a master transcription factor involved in jasmonate signaling, and activated the expression of the VITAMIN C DEFECTIVE1 (VTC1) and GLUTATHIONE SYNTHETASE1 (GSH1) gene families to enhance antioxidant biosynthesis. Consistent with this, the myb30 knockout mutant showed increased sensitivity to submergence, which was partially rescued by overexpression of VTC1 or GSH1. Thus, our findings uncover the mechanism by which the COP1-MYB30 module integrates light signals with cellular oxidative homeostasis to coordinate plant responses to postsubmergence stress.

Prefrontal cortex neural activity predicts reduction of non-suicidal self-injury in adolescents with major depressive disorder: An event related potential study.

Background: Non-suicidal self-injury (NSSI) is common in adolescent MDD, which is also a risk factor for suicide. However, there is few research on biomarkers and predictors about treatment response of NSSI. The purpose of this study was to find the difference of P300 between adolescent MDD with NSSI and healthy controls, and to explore whether the baseline electrophysiological level can predict the change of NSSI after treatment. Methods: We collected 62 first-episode drug-naïve MDD adolescents with NSSI (MDD with NSSI group) and 44 healthy controls (HC group). The demographic data, HAMD score, self-injury frequency and electrophysiological level of NSSI group and HC group were collected. The HAMD score, frequency of NSSI in was also collected after 8 weeks of antidepressant treatment. Results: Compared to HC, the latency of the N2, P3a, and P3b components were significantly prolonged, whereas the amplitude of P3a and P3b were decreased in the MDD with NSSI group (P < 0.001). The frequency of self-injury decreased significantly after treatment (P < 0.001). Regression analysis showed that the amplitudes of P3b had a significant positive predictive effect on the rate of change of NSSI frequency after 8 weeks. Conclusion: P3b at baseline can be used as potential predictor for the reduction of NSSI in adolescent MDD.

Identification and characterization of putative effectors from Plasmodiophora brassicae that suppress or induce cell death in Nicotiana benthamiana.

Clubroot, caused by Plasmodiophora brassicae, is a major disease of crucifers. Effector proteins are important virulence factors in host recognition of pathogens and the interactions between pathogens and hosts. Secretory proteins, as effector candidates, have been studied in the interaction between Plasmodiophora brassicae and its hosts. In this study, 518 secretary proteins were screened from the Plasmodiophora brassicae genome. A total of 63 candidate effectors that induce or suppress cell death were identified using agroinfiltration-mediated transient expression in Nicothiana benthamiana. The candidate effectors, Pb4_102097 and Pb4_108104 showed high expressing level in the stage of rest spore maturity, could induce cell death and were associated with H2O2 accumulation in N. benthamiana leaves. In addition, 55 candidate effectors that could suppress BAX (Bcl-2-associated X protein) induced cell death, and 21 out of which could suppress the immunity caused by bacterial pathogen Pseudomonas syringae pv. tomato strain DC3000 expressing avrRps4 in Arabidopsis. Based on the expression pattern in different stages, 28 candidate effectors showed high expression levels during the primary and secondary infection stage. Five candidate effectors containing the RXLR motif functioned in the cytoplasm and cell membrane.

Age Specific Risks of Uterine Cancer in Type 2 Diabetes and Associated Comorbidities in Taiwan.

Introduction: The global incidence of uterine cancer has increased substantially in recent decades. We evaluated if the trend of increasing prevalence of diabetes mellitus (DM) and obesity are attributed to the development of uterine cancer. Methods: Using data derived from the National Health Insurance database and Taiwan Cancer Registry, multivariate Cox proportional hazards regression models were adapted to analyze the risk factors of uterine cancer with potential confounding variables. Results: There were a total of 5,104,242 women aged 30−70 years enrolled in the study and 147,772 of them were diagnosed with DM during 2005−2007. In a total of 11 years of follow-up, 14,398 subjects were diagnosed with uterine cancer. An elevated risk of uterine cancer was observed in women with DM of all ages (HR 1.66, 95% CI 1.53−1.81, p < 0.0001). The effect of DM was highest at age 30−39 years (RR 3.05, 95% CI 2.35−3.96, p < 0.0001). In the group of <50 years old, DM patients had at least a twofold higher risk of developing uterine cancer (HR 2.39, 95% CI 2.09−2.74, p < 0.0001). Subjects among all ages diagnosed with polycystic ovary syndrome (PCOS) (HR 2.91, 95% CI 2.47−3.42, p < 0.0001), obesity (HR 2.13, 95% CI 1.88−2.41, p < 0.0001), and those undergoing hormone replacement therapy (HRT) (HR 1.60, 95% CI 1.33−1.93, p < 0.0001) were also positively associated with uterine cancer. Positive associations of hyperlipidemia (HR 1.33, 95% CI 1.22−1.46, p < 0.0001) and statin use (HR 1.27, 95% CI 1.12−1.44, p = 0.0002) on uterine cancer were only observed in subjects <50 years. On the contrary, hyperlipidemia was negatively associated with uterine cancer in subjects ≥50 years (HR 0.91, 95% CI: 0.84−0.98, p = 0.0122). Conclusions: DM is in general the most important risk factor for uterine cancer, especially in premenopausal women. Obesity, PCOS, HPL, statin use, and HRT were also associated with uterine cancer in subjects younger than 50 years. Premenopausal women with DM and respective comorbidities should be aware of the development of uterine cancer.

Identification and Characterization of Circular RNAs in Brassica rapa in Response to Plasmodiophora brassicae.

Plasmodiophora brassicae is a soil-borne pathogen that attacks the roots of cruciferous plants and causes clubroot disease. CircRNAs are noncoding RNAs, widely existing in plant and animal species. Although knowledge of circRNAs has been updated continuously and rapidly, information about circRNAs in the regulation of clubroot disease resistance is extremely limited in Brassica rapa. Here, Chinese cabbage (BJN 222) containing clubroot resistance genes (CRa) against P. brassicae Pb4 was susceptible to PbE. To investigate the mechanism of cicRNAs responsible for clubroot disease resistance in B. rapa, circRNA-seq was performed with roots of 'BJN 222' at 0, 8, and 23 days post-inoculated (dpi) with Pb4 and PbE. A total of 231 differentially expressed circRNAs were identified between the groups. Based on the differentially expressed circRNAs, the circRNA-miRNA-mRNA network was constructed using the target genes directly or indirectly related to plant resistance. Upregulated novel_circ_000495 suppressed the expression of miR5656-y, leading to the upregulation of Bra026508, which might cause plant resistance. Our results provide new insights into clubroot resistance mechanisms and lay a foundation for further studies exploring complex gene regulation networks in B. rapa.

Exploring the potential of thyroid hormones to predict clinical improvements in depressive patients: A machine learning analysis of the real-world based study.

BACKGROUND: Although undergoing antidepressant treatments, many patients continue to struggle with chronic depression episode. Seeking the potential biomarkers and establishing a predictive model of clinical improvements is vital to optimize personalized management of depression. Mounting evidence showed thyroid hormones changes are central to leading paradigms of depression. METHODS: Here, we conducted a real-world based retrospective study using clinical and biochemical data of 2086 depressive inpatients during period of 2014-2020. We first performed regression analyses to evaluate the contributing effect of free triiodothyronine (FT3), free thyroxine (FT4) and thyroid stimulating hormone (TSH) in predicting the clinical outcomes of depression. Then we established 7 predictive models using different combination of such hormones by supervised learning methods and tested the actual prediction efficacy on clinical outcomes, in order to select the one with the best predictive power. RESULTS: The results showed that lower values of FT3 and FT4 can both predict a poor clinical outcome in depression. Further, a model with the best performance was selected (sensitivity=0.91, specificity=0.79, and ROC-AUC=0.86), including the values of FT3 and FT4, and the scores of Hamilton Depression Scale (HAMD) and Hamilton Anxiety Scale (HAMA) as features. LIMITATIONS: The predictive model requires further external validation, and multi-center researches to confirm its clinical applicability. CONCLUSIONS: Our findings present a crucial role of thyroid measurements in predicting clinical outcomes of depression. Assessment of thyroid hormone should be extended to routine practice settings to determine which patients should be most in need of earlier or intensive interventions for preventing continued dysfunction.

SINAT E3 Ubiquitin Ligases Mediate FREE1 and VPS23A Degradation to Modulate Abscisic Acid Signaling.

In plants, the ubiquitin-proteasome system, endosomal sorting, and autophagy are essential for protein degradation; however, their interplay remains poorly understood. Here, we show that four Arabidopsis (Arabidopsis thaliana) E3 ubiquitin ligases, SEVEN IN ABSENTIA OF ARABIDOPSIS THALIANA1 (SINAT1), SINAT2, SINAT3, and SINAT4, regulate the stabilities of FYVE DOMAIN PROTEIN REQUIRED FOR ENDOSOMAL SORTING1 (FREE1) and VACUOLAR PROTEIN SORTING23A (VPS23A), key components of the endosomal sorting complex required for transport-I, to modulate abscisic acid (ABA) signaling. GFP-SINAT1, GFP-SINAT2, and GFP-SINAT4 primarily localized to the endosomal and autophagic vesicles. SINATs controlled FREE1 and VPS23A ubiquitination and proteasomal degradation. SINAT overexpressors showed increased ABA sensitivity, ABA-responsive gene expression, and PYRABACTIN RESISTANCE1-LIKE4 protein levels. Furthermore, the SINAT-FREE1/VPS23A proteins were codegraded by the vacuolar pathway. In particular, during recovery post-ABA exposure, SINATs formed homo- and hetero-oligomers in vivo, which were disrupted by the autophagy machinery. Taken together, our findings reveal a novel mechanism by which the proteasomal and vacuolar turnover systems regulate ABA signaling in plants.

Association between acrylamide exposure and sex hormones in males: NHANES, 2003-2004.

INTRODUCTION: Acrylamide is widely present in heat-processed food, cigarette smoke and environment. Reproductive toxicity was reported in animals treated with acrylamide, particularly in males. The reproductive toxicity of acrylamide and its active metabolite, glycidamide, was reported to be mainly mediated through DNA damage in spermatocytes. However, the effect of acrylamide on sex hormones in men is unknown. METHODS: There were 468 male subjects (age ≧ 12 years) enrolled to determine the relationships between hemoglobin adducts of acrylamide (HbAA) and hemoglobin adducts of glycidamide (HbGA) with several sex hormones using the National Health and Nutrition Examination Survey (NHANES), 2003 to 2004. All potential confounding variables in the data set were properly adjusted. RESULTS: We found that one unit increase in the natural log-transformed HbAA level was associated with an increase in natural log transformed serum inhibin B level by 0.10 (SE = 0.05; P = 0.046), and natural log transformed serum sex hormone binding globulin (SHBG) by 0.15 (SE = 0.15; P = 0.036). With respect to HbGA, one unit increase in the natural log-transformed HbGA level was associated with an increase in natural log transformed serum anti-Müllerian Hormone (AMH) level by 0.31 (SE = 0.00; P = 0.003). CONCLUSION: In this representative cohort, we identified positive associations between acrylamide exposure and several sex hormones in men. The HbAA is positively associated with inhibin B and SHBG, and HbGA is positively associated with AMH. Other than genotoxicity, our findings suggested that altered sex hormones might also play a role in acrylamide-related reproductive toxicity in males.

Association among total serum isomers of perfluorinated chemicals, glucose homeostasis, lipid profiles, serum protein and metabolic syndrome in adults: NHANES, 2013-2014.

Perfluorinated chemicals (PFCs) have been used widely in consumer products manufacture. Recent in vitro as well as animal studies have found that there are different toxicity and pharmacokinetic profiles between isomers of perfluorooctanoic acid (PFOA) and/or perfluorooctane sulfonate (PFOS). However, the differential effects of linear or branched PFOA/PFOS isomers on human beings have never been reported. Herein, we examined 1871 adult subjects (age older than 18 years) from the National Health and Nutrition Examination Survey (NHANES) 2013-2014 to determine the association between the isomers of PFOA/PFOS and serum biochemistry profiles, including glucose, lipids, protein and components of metabolic syndrome (MS). The results showed that for PFOA, increased linear PFOA was associated with increases in total cholesterol, serum albumin and an enhancement of ß cell function as well as a decrease in the serum globulin. Increased branched PFOA was significantly associated with increased fasting glucose. All isomers of PFOA were positively associated with high-density lipoprotein-cholesterol (HDL-C) and negatively associated with glycohemoglobin (HbA1C). The branched PFOS was positively associated with ß cell function and inversely associated with serum globulin. Both linear and branched isomers of PFOS were positively associated with the total protein and albumin. The increased branched PFOA was associated with less HDL-C insufficiency defined by the National Cholesterol Education Program Third Adult Treatment Panel (NCEP-ATP III) MS criteria, whereas the increased concentrations of serum total and linear PFOS were associated with less hypertriglyceridemia by the NCEP-ATP III. In conclusion, serum isomers of PFOA and PFOS were associated with glucose homeostasis, serum protein as well as lipid profiles; they were also indicators of MS. This may suggest that there is a distinct difference in the toxicokinetics of the isomers of PFOA and PFOS. Further clinical and animal studies are warranted to clarify the putative causal relationships between isomers and biochemical alterations.