The correlation between cumulative burden of mental disorders and self-harm, shame, and insight in young female patients with schizophrenia.

This study delves into the correlation between the cumulative burden of mental disorders and self-harm, shame, and insight in young female patients with schizophrenia. A prospective randomized controlled study was used to recruit 62 female schizophrenia patients who met the recruitment conditions from January 2022 to December 2023. The participants were randomly divided into an experimental group (31 cases) and a control group (31 cases) using a computer-based random number distribution method. The experimental group underwent an 8-week Mindfulness-Based Cognitive Therapy (MBCT) intervention, while the control group received conventional treatment. Data was collected using the Modified EI-SHS scale, the Link's Stigma Scale (LSS), the Five-factor Mindfulness Scale (FFMQ), and the Self-awareness and Therapeutic Attitude Questionnaire (ITAQ) before and after the intervention. One-way ANOVA and repeated measure ANOVA were used to compare and analyze the two groups of data. The experimental group exhibited a significant reduction in EI-SHS and LSS scores (100.26 ± 11.48 vs. 88.35 ± 10.09, 112.81 ± 12.30 vs. 100.50 ± 13.52, p < 0.01), coupled with significant increase in FFMQ and ITAQ scores (113.77 ± 12.25 vs. 128.31 ± 14.09, 14.03 ± 4.18 vs. 17.30 ± 2.96, p < 0.01). A positive correlation was found between overall stigma scores and mood disorder scores (r = 0.379, P < 0.011). Correlation analysis revealed a negative correlation between mindfulness (self-awareness) and stigma (r = -0.128, P = 0.025). MBCT effectively reduced stigma in young women with schizophrenia and improved coping tendencies, cognitive status, and attitudes toward mental illness, ultimately reducing the cumulative burden of mental disorders and self-harm in these patients. Increased levels of mindfulness correspond to improved cognitive status and a more positive attitude toward treatment for mental illness. It is of great value to promote MBCT in female patients with schizophrenia.

CircCHMP5 Contributes to Ox-LDL-induced Endothelial Cell Injury Through the Regulation of MiR-532-5p/ROCK2 axis.

BACKGROUND: Aberrant expression of circular RNA (circRNA) has been demonstrated to be related to atherosclerosis (AS) formation. However, the mechanism of circCHMP5 (also known as hsa_circ_0003575) in AS formation remains unclear. METHODS: Oxidized low-density lipoprotein (ox-LDL) was used to treat human umbilical vein endothelial cells (HUVECs) to construct a cell injury model. The expression level of circCHMP5, miR-532-5p, and Rho-associated protein kinase 2 (ROCK2) was measured using quantitative real-time PCR. Cell cycle, apoptosis, proliferation, and angiogenesis were determined by flow cytometry, 5-ethynyl-2'-deoxyuridine (EdU) assay, and tube formation assay. In addition, the protein expression of apoptosis markers, inflammation factors, and ROCK2 was detected by western blot analysis. The interaction between miR-532-5p and circCHMP5 or ROCK2 was assessed by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. RESULTS: Our results indicated that circCHMP5 was overexpressed in ox-LDL-induced HUVECs. CircCHMP5 knockdown promoted cell cycle, proliferation, and angiogenesis while inhibiting apoptosis and inflammation in ox-LDL-induced HUVECs. MiR-532-5p could be sponged by circCHMP5, and its inhibitor reversed the negative regulation of si-circCHMP5 on ox-LDL-induced HUVECs injury. ROCK2, a target of miR-532-5p, reversed the inhibition effect of miR-532-5p on ox-LDL-induced HUVECs injury. Furthermore, we confirmed that circCHMP5 upregulated ROCK2 by sponging miR-532-5p. CONCLUSION: To sum up, our data showed that circCHMP5 regulated the miR-532-5p/ROCK2 axis to accelerate ox-LDL-induced HUVECs injury, confirming that circCHMP5 might be a potential target for AS treatment.

HDAC9 exacerbates myocardial infarction via inactivating Nrf2 pathways.

OBJECTIVES: Myocardial infarction (MI) is the leading cause of death worldwide. Histone deacetylases (HDACs) collectively participate in the initiation and progression of heart diseases, including MI. This study aimed to investigate the roles of histone deacetylase 9 (HDAC9) in the development of MI. METHODS: In vivo and in vitro assays were conducted to determine the effects of HDAC9 on heart function and MI. qRT-PCR was applied to determine the mRNA level. Western blot was performed for protein expression. Immunofluorescence was applied to detect the fluorescence tensity of Myog and Myod. CCK-8, flow cytometry and transwell assays were carried out for function analysis. KEY FINDINGS: HDAC9 was upregulated in MI models in vivo and in vitro. Downregulated HDAC9 modulated the changes in left ventricle ejection fraction (LVEF), left ventricle fractional shortening (LVFS) and left ventricular end-diastolic diameter (LVEDD) and left ventricular end-systolic diameter (LVESD). Moreover, HDAC9 knockdown activated NFE2-related factor 2 (Nrf2)/Keap1/HO-1 pathways. Additionally, HDAC9/Nrf2 axis modulated the proliferation, apoptosis and myogenesis of cardiomyocytes. CONCLUSIONS: Taken together, HDAC9 knockout induced the activation of Nrf2 and protected heart from MI injury. Thus, the HDAC9/Nrf2 axis can be a novel marker for the treatment of MI.

Occurrence, behavior, and fate of organophosphate esters (OPEs) in subtropical paddy field environment: A case study in Nanning City of South China.

Occurrence, behavior, and fate of 11 OPEs in multiple environmental matrices, which include air, rainwater, dustfall, paddy soil, irrigation water, and rice plants from nine subtropical paddy fields of South China, were investigated. The total concentrations of 11 OPEs (∑11OPEs) in all matrices are generally higher in the urban areas than in rural areas, and they are higher in summer than in fall. However, both urban and rural areas showed a similar composition profile of OPEs, indicating that the OPEs come from similar sources in the two areas. Except for irrigation water, significant positive correlations of ∑11OPEs were observed between air and the other five matrices. The exchange and partition of OPEs among air, soil, and water demonstrate that most of OPEs were transferred from air into water and soil, and from water into soil. Thus, the air may be an important source of OPEs in the paddy fields, and the soil may act as a principal environmental reservoir of OPEs. The contribution of air-soil exchange, atmospheric deposition (rainwater plus dustfall), and irrigation water to the total input fluxes of OPEs (2100 ± 980 ng/m2/day) reached an average of 19%, 38% (37% + 1%), and 43%, respectively. The water (rainwater plus irrigation water) is the primary medium transferring the OPEs into the paddy fields and contributed to the input flux by 80%. Output flux of OPEs via mature rice plants was about 220 µg/m2, 2% of which were presented in rice, and the remaining 98% may be re-released into the environment through the pathway of straw turnover or burning. Dietary exposure via rice was much higher than inhalation exposure, dust ingestion, and dermal absorption via dust. However, no data shows that all of the intakes via the four exposure pathways could cause the risks to human health at present.

Analysis of the clinical value of fractional flow reserve for prognosis evaluation of patients of percutaneous coronary intervention.

We investigated the clinical value of fractional flow reserve (FFR) for the prognostic evaluation of patients with percutaneous coronary intervention. We enrolled 120 patients who were admitted to the hospital to undergo percutaneous coronary intervention for acute coronary syndromes between May 2014 and June 2015. The 120 patients were divided into two groups, the observation group and the control group, according to the post-surgery level of FFR. Each cohort contained 60 patients. These patients were divided into the occurrence group (n=45) and the non-occurrence group (n=75), classified according to the occurrence of major adverse cardiovascular events (MACE). There were no statistically significant differences in the comparison of the occurrence rate of MACE within 30 days after surgery, such as lethal or non-lethal myocardial infarction or non-lethal cerebrovascular events, between the observational group and the control group (P>0.05). For the observation group, the 1-year survival cases were 56 with a survival rate of 93.3%, and 2-year survival cases were 50 with a survival rate of 83.3%. In the control group, the 1-year and 2-year survival cases were respectively 55 and 49 (survival rate of 91.7 and 81.7%). The occurrence rates of hyperlipidemia and ratio of patients with a history of smoking and drinking in the occurrence group were significantly higher than those in the non-occurrence group (P<0.05). The mean arterial pressure in the occurrence group was significantly higher than that in the non-occurrence group (P<0.05). Heart rate in the occurrence group is significantly faster than that in the non-occurrence group (P<0.05) and the stenosis degree in the occurrence group was significantly higher than that in the non-occurrence group (P<0.05). The left ventricular ejection fraction (LVEF) before surgery in the occurrence group was significantly lower than that in the non-occurrence group (P<0.05). There were no remarkable differences in comparison of the pre-treatment FFR between the occurrence group and the non-occurrence group (P>0.05), but the post-treatment FFR in the occurrence group was significantly lower than that in the non-occurrence group (P<0.05). Increased blood fat, a history of smoking and drinking, augmented mean arterial pressure, accelerated heart rate, severe coronary artery stenosis and the remarkably decreased LVEF were all identified as independent risk factors leading to major adverse myocardial events. The sum of specificity and sensitivity of treatment reached the peak when the post-surgery FFR was 0.875, the calculated sensitivity was 82.4%, and the specificity was 50.8%. In conclusion, measurement of FFR after percutaneous coronary intervention could not only effectively evaluate the target vessel revascularization, but also predict the occurrence of major adverse myocardial events 1 year after surgery, which could serve as the guidance for clinical treatment.

Hormetic Effects of Trifloxystrobin on Aggressiveness of Sclerotinia sclerotiorum.

Sclerotinia sclerotiorum is a devastating ascomycete plant pathogen with an extremely wide host range. Fungicides are still the mainstay for control of this pathogen, and stimulations to mycelial growth and aggressiveness by subtoxic doses of fungicides carbendazim and dimethachlon have been reported. The present study assessed hormetic effects of the quinone outside inhibitor (QoI) fungicide trifloxystrobin on aggressiveness of S. sclerotiorum. Trifloxystrobin at 0.0001, 0.0005, and 0.001 µg/ml exerted significant stimulatory effects on aggressiveness to potted rapeseed plants, and the highest percent stimulation were 20.5 and 24.2% for isolates HB15 and SX11, respectively. At 18 h postinoculation (HPI), initial necrotic lesions were visible to the naked eye on leaves treated with trifloxystrobin, whereas no obvious disease symptoms were discerned for the nontreated control. At 24, 36, and 48 HPI, aggressiveness stimulation was more obvious than at 18 HPI. Scanning electron microscopic observations demonstrated that no mycelia were detected on the nontreated leaves at 4 HPI; by contrast, mycelia were observed on leaves treated with trifloxystrobin at 0.0001 µg/ml. At 8 and 12 HPI, there were more mycelia and infecting hyphae on the treated leaves than on the nontreated control. These results indicated that fungal stimulation had occurred in the first 4 and 8 HPI, suggesting that direct stimulation was likely to be the underlying mechanism for hormetic actions of trifloxystrobin. Pretreatment with trifloxystrobin did not significantly affect subsequent mycelial growth on PDA or aggressiveness to detached rapeseed leaves in the absence of trifloxystrobin. However, in the presence of trifloxystrobin, mycelial growth and aggressiveness were significantly (P < 0.05) greater for the pretreatment with trifloxystrobin at 0.003 and 0.03 µg/ml compared with the nonpretreatment control, indicating that a prior exposure to the fungicide may undermine its subsequent effectiveness. These studies will raise our awareness of fungicide hormesis and have important implications for judicious application of fungicides.

Time Course of Carbendazim Stimulation on Pathogenicity of Sclerotinia sclerotiorum Indicates a Direct Stimulation Mechanism.

Previous studies have demonstrated that subtoxic doses of carbendazim have a stimulatory effect on pathogenicity of Sclerotinia sclerotiorum on rapeseed plants. The present study focused on the time-course profile of the stimulatory effect and its relevance to stimulation mechanisms. At 12 h postinoculation (HPI), initial necrotic lesions were visible only for rapeseed leaves treated with carbendazim at 0.2 and 1 µg/ml, whereas no disease symptoms were observed for the nontreated control. At 18 HPI, carbendazim stimulation on pathogenicity was more obvious than at 12 HPI. Study with scanning electron microscopy demonstrated that no discernable differences in the development of disease symptoms could be detected at 8 HPI. However, at 12 HPI, necrotic symptoms of the epidermal cells were apparent only for leaves sprayed with carbendazim. These results indicated that stimulations on pathogenicity occurred in the first 12 h, implying that direct stimulation rather than overcompensation to the disruption of homeostasis was likely to be the underlying mechanism for pathogenicity stimulation. Greenhouse experiments showed that spraying carbendazim at 400 µg/ml on potted rapeseed plants had statistically significant (P < 0.05) stimulations on pathogenicity for inoculations at 1, 3, 5, and 7 days after application (DAA). The stimulation action eventually disappeared for inoculations at 14 DAA. Mycelia grown on potato dextrose agar (PDA) supplemented with carbendazim at 400 µg/ml were more pathogenic than the nontreated control. However, after additional growth of the mycelia on fungicide-free PDA for 2 days, the stimulatory effect disappeared completely, indicating that carbendazim was indispensable for pathogenicity stimulations. Studies on biochemical mechanisms indicated that cell-wall-degrading enzymes such as cellulase, pectinase, and polygalacturonase were not involved in pathogenicity stimulations. These results will advance our understanding of the nature and mechanisms of fungicide stimulation on fungal pathogenicity and, thus, are valuable for judicious applications of fungicides.

Pathogenicity Stimulation of Sclerotinia sclerotiorum by Subtoxic Doses of Carbendazim.

Sclerotinia sclerotiorum is a devastating ascomycete fungus capable of infecting more than 400 species of plants worldwide. Carbendazim has been a principal fungicide for control of this pathogen and high levels of carbendazim resistance have been reported in eastern China. In this study, stimulatory effect of subtoxic doses of carbendazim on pathogenicity of S. sclerotiorum was investigated. All seven field resistant isolates with EC50 values greater than 1,000 µg/ml exhibited stimulated pathogenicity toward detached leaves of rapeseed at subtoxic concentrations of carbendazim. Detailed studies on pathogenicity of two resistant isolates AH-17 and LJ-86 toward potted rapeseed plants and detached leaves demonstrated that carbendazim at 0.2 to 5 µg/ml could consistently stimulate significantly higher (P < 0.05) pathogenicity than the control. On potted rapeseed plants, the percent stimulations on pathogenicity ranged from 18.8 to 22.0% for isolate AH-17 and from 15.1 to 23.2% for isolate LJ-86. On detached leaves of rapeseed, the percent stimulations ranged from 18.7 to 31.29% for isolate AH-17 and from 16.7 to 24.3% for isolate LJ-86. Studies on stimulation mechanism indicated that secretion of oxalic acid and tolerance to oxidative stresses H2O2 and paraquat after exposed to subtoxic doses of carbendazim did not change significantly. These results have profound implications for judicious application of fungicides and sustainable management of fungicide resistance.

Baseline Sensitivity of Pyraclostrobin and Toxicity of SHAM to Sclerotinia sclerotiorum.

Sclerotinia sclerotiorum is a cosmopolitan plant pathogen notable for its wide host range. The quinone outside inhibitor (QoI) fungicide pyraclostrobin has not been registered for control of S. sclerotiorum in China. In this study, baseline sensitivity of pyraclostrobin was established based on effective concentration for 50% inhibition of mycelial growth (EC50) values of 153 isolates of S. sclerotiorum collected from five provinces of China and toxicity of alternative oxidase inhibitor salicylhydroxamic acid (SHAM) to S. sclerotiorum was determined. Results showed that the frequency distribution of EC50 values of the 153 isolates was unimodal but with a right-hand tail. The mean EC50 value was 0.1027 µg/ml and the range of EC50 values was 0.0124 to 0.6324 µg/ml. Applied as a preventive fungicide in pot experiments, pyraclostrobin at 5, 15, and 45 µg/ml provided control efficacies of 61, 77, and 100%, respectively. There was no positive cross-resistance between pyraclostrobin and carbendazim or dimethachlon. EC50 values for SHAM against four isolates of S. sclerotiorum were 44.4, 51.8, 54.4, and 68.7 µg/ml. SHAM at 20 µg/ml could significantly increase not only the inhibitory effect of pyraclostrobin on mycelial growth on potato dextrose agar media but also the control efficacy in planta. These results indicated that SHAM should not be added into artificial media in in vitro assay of S. sclerotiorum sensitivity to pyraclostrobin. This has broad implications for assay of sensitivity of fungal pathogen to QoI fungicides.

Stimulatory Effects of Sublethal Doses of Dimethachlon on Sclerotinia sclerotiorum.

Growth and virulence stimulations of sublethal doses of fungicides on plant-pathogenic fungi and oomycetes have been reported and the stimulatory effects are potentially relevant to plant disease management. Sclerotinia sclerotiorum is one of the most devastating and economically important necrotrophic fungal phytopathogens, capable of infecting more than 400 species of plants worldwide. In order to study stimulatory effects of sublethal doses of fungicides on S. sclerotiorum, 55 dimethachlon-sensitive isolates and 3 dimethachlon-resistant isolates of S. sclerotiorum were assayed to determine effects of sublethal doses of dimethachlon on mycelial growth rate on potato dextrose agar (PDA) media and virulence on oilseed rape plants. Results showed that all 3 dimethachlon-resistant isolates and 13 of the 55 sensitive isolates exhibited stimulatory responses to sublethal doses of dimethachlon. Dimethachlon-resistant isolates grew significantly (P < 0.05) faster on PDA media amended with dimethachlon at 0.5 to 4 µg/ml than on fungicide-free PDA media. As for virulence on detached leaves of oilseed rape plants, lesion diameters of dimethachlon-resistant isolates after growth on PDA media amended with dimethachlon at 0.5 to 2 µg/ml were significantly larger (P < 0.05) than the control. The maximum stimulatory effects were 42.40 to 59.80%. In pot experiments, for both dimethachlon-sensitive and -resistant isolates, significant (P < 0.05) virulence stimulations were observed after spraying with dimethachlon at a concentration of 2 µg/ml. After growing on dimethachlon-amended PDA media, H2O2 sensitivity of S. sclerotiorum decreased significantly (P < 0.05) compared with the nonamended PDA control.