Efficacy of Streptomyces murinus JKTJ-3 in Suppression of Pythium Damping-Off of Watermelon.

Damping-off caused by Pythium aphanidermatum (Pa) is one of the most destructive diseases for watermelon seedlings. Application of biological control agents against Pa has attracted the attention of many researchers for a long time. In this study, the actinomycetous isolate JKTJ-3 with strong and broad-spectrum antifungal activity was screened from 23 bacterial isolates. Based on the morphological, cultural, physiological, and biochemical characteristics as well as the feature of 16S rDNA sequence, isolate JKTJ-3 was identified as Streptomyces murinus. We investigated the biocontrol efficacy of isolate JKTJ-3 and its metabolites. The results revealed that seed and substrate treatments with JKTJ-3 cultures showed a significant inhibitory effect on watermelon damping-off disease. Seed treatment with the JKTJ-3 cultural filtrates (CF) displayed higher control efficacy compared to the fermentation cultures (FC). Treatment of the seeding substrate with the wheat grain cultures (WGC) of JKTJ-3 exhibited better control efficacy than that of the seeding substrate with the JKTJ-3 CF. Moreover, the JKTJ-3 WGC showed the preventive effect on suppression of the disease, and the efficacy increased with increase in the inoculation interval between the WGC and Pa. Production of the antifungal metabolite actinomycin D by isolate JKTJ-3 and cell-wall-degrading enzymes such as ß-1,3-glucanase and chitosanase were probably the mechanisms for effective control of watermelon damping-off. It was shown for the first time that S. murinus can produce anti-oomycete substances including chitinase and actinomycin D. This is the first report about S. murinus used as biocontrol agent against watermelon damping-off caused by Pa.

The complete mitochondrial genome of Fannia canicularis (Diptera: Fanniidae).

Fannia canicularis (Linnaeus, 1761) is a species from the family Fanniidae. In this study, we sequenced and analyzed the complete mitochondrial genome of F. canicularis for the first time. The circular mitogenome is 15,826 bp in length, and includes 13 protein-coding genes (PCGs), 22 transfer RNA genes, two ribosomal RNA genes, and a non-coding control region. The family Fanniidae formed a monophyletic clade in the phylogenetic tree based on 13 concatenated PCGs, sister to three other families in Diptera.

Corrigendum: Prevalence and Influencing Factors of Anxiety and Depression Symptoms in the First-Line Medical Staff Fighting Against COVID-19 in Gansu.

[This corrects the article DOI: 10.3389/fpsyt.2020.00386.].

The Attitude towards Preventive Measures and Knowledge of COVID-19 Inpatients with Severe Mental Illness in Economically Underdeveloped Areas of China.

Patients with severe mental illnesses (SMI) were at high risk of infection during Coronavirus Diseases 2019 (COVID-19) pandemic. This study examined hospitalized SMI patients' attitude and knowledge towards the COVID-19 infection. A cross-sectional survey was conducted in five psychiatric hospitals located in Gansu province, the most economically underdeveloped area in China. Patients' attitude towards preventive measures and knowledge of COVID-19 were measured by a self-report questionnaire. A total of 925 hospitalized patients with SMI were recruited. Of them, 84.8% (95%CI: 82.4%-87.1%) had positive attitudes towards preventive measures of the COVID-19 outbreak. Being married (OR: 1.55, 95%CI: 1.05-2.30) and a higher educational level (OR: 1.63, 95%CI: 1.12-2.38) were independently associated with positive attitudes towards COVID-19 preventive measures, whereas higher educational level was associated with better knowledge of the COVID-19 outbreak (ß: 0.231, P < 0.001). Patients mainly received COVID-19 relevant knowledge from public media (58.9%), followed by their clinicians (33.2%). Most hospitalized SMI patients in economically underdeveloped areas in China showed positive attitudes towards COVID-19 preventive measures. However, public health education on COVID-19 relevant knowledge by mental health professionals was inadequate to reduce the risk of transmission and infection.

Prevalence and Influencing Factors of Anxiety and Depression Symptoms in the First-Line Medical Staff Fighting Against COVID-19 in Gansu.

BACKGROUND: The outbreak of novel coronavirus pneumonia (COVID-19) has brought enormous physical and psychological pressure on Chinese medical staff. It is extremely important to understand the prevalence and influencing factors of anxiety and depression symptoms in first-line anti-epidemic medical staff and their coping styles for these negative emotions. METHODS: A cross-sectional survey was conducted in Gansu (China), with a questionnaire packet which consisted of the self-rating anxiety scale (SAS), self-rating depression scale (SDS), and the simplified coping style questionnaire (SCSQ). A total of 79 doctors and 86 nurses participated in the survey. Correlation analysis was performed to explore the relationship between SAS, SDS, and SCSQ score. A linear regression model was used to determine the influencing factors for anxiety or depression symptoms. RESULTS: The prevalence rates of anxiety and depression symptoms among doctors was 11.4% and 45.6%, respectively. History of depression or anxiety (T=-2.644, p= 0.010, 95%CI: -10.514~-1.481) was shown to be a risk factor for anxiety symptoms in doctors, while being male (T=2.970, p=0.004, 95%CI: 2.667~13.521) was a protective factor for depression. The prevalence rate of anxiety and depression symptoms among nurses was 27.9% and 43.0%, respectively. History of depression or anxiety was a common risk factor for anxiety symptoms (T=-3.635, p=0.000, 95%CI: -16.360~-4.789) and depression symptoms (T=-2.835, p=0.005, 95%CI:-18.238~-3.254) in nurses. The results of partial correlation analysis (controlled for gender and history of depression or anxiety) indicated that the total score of positive coping was negatively correlated with the total score of anxiety (r=-0.182, p=0.002) and depression (r=-0.253, p=0.001). CONCLUSIONS: The first-line anti-epidemic medical staff have high anxiety and depression symptoms and adopting positive coping styles will help to improve their negative emotions.

Unmedicated patients with schizophrenia in economically underdeveloped areas of China.

OBJECTIVES: Untreated schizophrenia commonly leads to poor prognosis. The medication treatment rate of schizophrenia patients in economically underdeveloped areas of China has not been well-studied. This study aimed to examine the pattern of unmedicated schizophrenia patients in economically underdeveloped rural and urban areas of China. METHOD: A total of 4240 schizophrenia patients in Lanzhou (1720 rural and 2520 urban patients) registered in the community mental-health service system in Lanzhou, Gansu province were included. Their socio-demographic and clinical characteristics including medication treatment status were collected and analyzed. RESULTS: The proportion of unmedicated schizophrenia patients was 22.5% (n = 953) in the whole sample, with 32.3% (556/1720) in rural and 15.8% (397/2520) in urban patients (X2=161.1, P < 0.001). Multiple logistic regression analyses revealed that unmedicated schizophrenia patients in rural area were more likely to be older (OR=1.02, 95%CI: 1.01-1.03), male (OR=1.35, 95%CI: 1.07-1.71), unmarried (OR=0.71, 95%CI: 0.55-0.91), and have lower educational level (OR=0.39, 95%CI: 0.24-0.65), longer illness duration (OR=1.01, 95%CI: 1.00-1.02) and less frequent admissions (OR=0.46, 95%CI: 0.38-0.54). In contrast, unmedicated patients in urban area were more likely to be older (OR=1.01, 95%CI: 1.00-1.02), unmarried (OR=0.77, 95%CI: 0.61-0.98), employed (OR=2.38, 95%CI: 1.87-3.04), and have lower educational level (OR=0.49, 95%CI: 0.37-0.65), better financial status (OR=0.60, 95%CI: 0.48-0.76) and less frequent admissions (OR=0.81, 95%CI: 0.75-0.87). CONCLUSIONS: The rate of unmedicated schizophrenia patients is high in economically underdeveloped areas of China, particularly in rural areas. Effective policies and measures should be implemented urgently to improve the treatment rate in this population.

Macrophage-Mediated Glial Cell Elimination in the Postnatal Mouse Cochlea.

Hearing relies on the transmission of auditory information from sensory hair cells (HCs) to the brain through the auditory nerve. This relay of information requires HCs to be innervated by spiral ganglion neurons (SGNs) in an exclusive manner and SGNs to be ensheathed by myelinating and non-myelinating glial cells. In the developing auditory nerve, mistargeted SGN axons are retracted or pruned and excessive cells are cleared in a process referred to as nerve refinement. Whether auditory glial cells are eliminated during auditory nerve refinement is unknown. Using early postnatal mice of either sex, we show that glial cell numbers decrease after the first postnatal week, corresponding temporally with nerve refinement in the developing auditory nerve. Additionally, expression of immune-related genes was upregulated and macrophage numbers increase in a manner coinciding with the reduction of glial cell numbers. Transient depletion of macrophages during early auditory nerve development, using transgenic CD11bDTR/EGFP mice, resulted in the appearance of excessive glial cells. Macrophage depletion caused abnormalities in myelin formation and transient edema of the stria vascularis. Macrophage-depleted mice also showed auditory function impairment that partially recovered in adulthood. These findings demonstrate that macrophages contribute to the regulation of glial cell number during postnatal development of the cochlea and that glial cells play a critical role in hearing onset and auditory nerve maturation.

Heptanol application to the mouse round window: a model for studying cochlear lateral wall regeneration.

OBJECTIVE: Identify cells supporting cochlear lateral wall regeneration. STUDY DESIGN: Prospective controlled trial. SETTING: Laboratory. Human presbyacusis occurs, in part, secondary to age-related degeneration of cochlear lateral wall structures such as the stria vascularis and spiral ligament fibrocytes. This degeneration is likely linked to the diminished regenerative capacity of lateral wall cells with age. While lateral wall regeneration is known to occur after an acute insult, this process remains poorly understood and the cells capable of self-replication unidentified. We hypothesized that spiral ligament fibrocytes constitute these proliferative cells. SUBJECTS AND METHODS: To test the hypothesis, an acute ototoxic insult was created in 65 normal-hearing, young adult mice via cochlear exposure to heptanol. Sacrifice occurred at 1 to 60 days posttreatment. Auditory brainstem responses, 5-ethynyl-2'-deoxyuridine assay, and immunostaining were used to assess regeneration. RESULTS: Posttreatment hearing thresholds were elevated in nearly all treated mice. Selective fibrocyte apoptosis and strial injury were observed at the time of peak hearing loss around 1 to 7 days posttreatment. Cellular proliferation was detected in the region of type II fibrocytes during this time. Hearing thresholds plateaued at 7 days posttreatment followed by a significant recovery of both hearing and morphologic appearance. Permanent outer hair cell degeneration was observed. CONCLUSIONS: Heptanol application to the round window of young adult mice is a rapid, selective, and reliable technique for investigating proliferation in the cochlear lateral wall. The data indirectly showed that spiral ligament fibrocytes may be the proliferative cells of the cochlear lateral wall. Further studies of this process are needed.

Analysis of miR-376 RNA cluster members in the mouse inner ear.

Mutations in phosphoribosyl pyrophosphate synthetase 1 (PRPS1) are associated with a spectrum of non-syndromic to syndromic hearing loss. PRPS1 transcript levels have been shown to be regulated by the microRNA-376 genes. The long primary RNA transcript of the miR-376 RNA cluster members undergo extensive and simultaneous A → I editing at one or both of two specific sites (+4 and +44) in particular human and mouse tissues. The PRPS1 gene, which contains target sites for the edited version of miR-376a-5p within its 3'UTR, has been shown to be repressed in a tissue-specific manner. To investigate whether the transcription of Prps1 is regulated by miR-376 cluster members in the mouse inner ear, we first quantified the expression of the mature miR-376 RNAs by quantitative real-time-PCR. The spatio-temporal patterns of miR-376 expression were assessed by in situ hybridization. Finally, we examined whether A →I editing of pri-miR-376 RNAs occurs in mouse inner ear by direct sequencing. Our data showed that the miR-376a-3p, b-3p, c-3p are present in mouse embryonic inner ears and intensive expression of miR-376a-3p/b-3p was detected in the sensory epithelia and ganglia of both auditory and vestibular portions of the inner ear. In adult inner ear, the expression of miR-376a-3p/b-3p is restricted within ganglion neurons of auditory and vestibular systems as well as the cells in the stria vascularis. Only unedited pri-miR-376 RNAs were detected in the cochlea suggesting that the activity of PRPS1 in the inner ear may not be regulated through the editing of miR-376 cluster.

Role of stromal cell-derived factor-1 expression in the injured mouse auditory nerve.

OBJECTIVE: The degeneration of hair cells and spiral ganglion neurons (SGNs) is an important pathologic process in the development of sensorineural hearing loss. In a murine model, predictable and reproducible damage to SGNs occurs through the application of ouabain to the round window. Recent evidence has shown that the chemokine stromal cell-derived factor-1 (SDF-1) is a potent chemoattractant of hematopoietic stem cells (HSCs) and provides trophic support to injured tissues during development and maturation. The hypothesis for the current study is that expression of SDF-1 plays an important role in protecting SGNs and preventing further degeneration in the setting of cochlear injury. STUDY DESIGN: Prospective, controlled. SETTING: Academic research laboratory. SUBJECT AND METHODS: Auditory brainstem response (ABR) and the expression of SDF-1 mRNA and protein were examined 1, 3, 7, 14, and 30 days after application of ouabain in 35 adult mice. RESULTS: Following ouabain application, real-time reverse-transcription polymerase chain reaction for SDF demonstrates increased mRNA expression following ouabain injury in nontransplanted mice. A significant increase in SDF protein expression was also observed using immunolabeling techniques and Western blot analysis. CONCLUSIONS: SDF-1 expression is increased in the auditory nerve following cochlear injury. Further knowledge about the cochlear microenvironment, including SDF-1, is critical to maximizing HSC engraftment in the injured cochlea and providing a therapeutic option for sensorineural hearing loss.

Sox2 up-regulation and glial cell proliferation following degeneration of spiral ganglion neurons in the adult mouse inner ear.

In the present study, glial cell responses to spiral ganglion neuron (SGN) degeneration were evaluated using a murine model of auditory neuropathy. Ouabain, a well-known Na,K-ATPase inhibitor, has been shown to induce SGN degeneration while sparing hair cell function. In addition to selectively removing type I SGNs, ouabain leads to hyperplasia and hypertrophy of glia-like cells in the injured auditory nerves. As the transcription factor Sox2 is predominantly expressed in proliferating and undifferentiated neural precursors during neurogenesis,we sought to examine Sox2 expression patterns following SGN injury by ouabain. Real-time RT-PCR and Western blot analyses of cochlea indicated a significant increase in Sox2 expression by 3 days posttreatment with ouabain. Cells incorporating bromodeoxyuridine(BrdU) and expressing Sox2 were counted in the auditory nerves of control and ouabain-treated ears. The glial phenotype of Sox2+cells was identified by two neural glial markers: S100 and Sox10. The number of Sox2+ glial cells significantly increased at 3 days post-treatment and reached its maximum level at 7 days post-treatment. Similarly,the number of BrdU+ cells increased at 3 and 7 days post-treatment in the injured nerves. Quantitative analysis with dual-immunostaining procedures indicated that about 70% of BrdU+ cells in the injured nerves were Sox2+ glial cells. These results demonstrate that up-regulation of Sox2 expression is associated with increased cell proliferation in the auditory nerve after injury.

Adrenomedullin improves cardiac function and prevents renal damage in streptozotocin-induced diabetic rats.

Adrenomedullin (AM) is a potent vasodilating peptide and is involved in cardiovascular and renal disease. In the present study, we investigated the role of AM in cardiac and renal function in streptozotocin (STZ)-induced diabetic rats. A single tail-vein injection of adenoviral vectors harboring the human AM gene (Ad.CMV-AM) was administered to the rats 1-wk post-STZ treatment (65 mg/kg iv). Immunoreactive human AM was detected in the plasma and urine of STZ-diabetic rats treated with Ad.CMV-AM. Morphological and chemical examination showed that AM gene delivery significantly reduced glycogen accumulation within the hearts of STZ-diabetic rats. AM gene delivery improved cardiac function compared with STZ-diabetic rats injected with control virus, as observed by decreased left ventricular end-diastolic pressure, increased cardiac output, cardiac index, and heart rate. AM gene transfer significantly increased left ventricular long axis (11.69 +/- 0.46 vs. 10.31 +/- 0.70 mm, n = 10, P < 0.05) and rate of pressure rise and fall (+6,090.1 +/- 597.3 vs. +4,648.5 +/- 807.1 mmHg/s), (-4,902.6 +/- 644.2 vs. -3,915.5 +/- 805.8 mmHg/s, n = 11, P < 0.05). AM also significantly attenuated renal glycogen accumulation and tubular damage in STZ-diabetic rats as well as increased urinary cAMP and cGMP levels, along with increased cardiac cAMP and Akt phosphorylation. We also observed that delivery of the AM gene caused an increase in body weight along with phospho-Akt and membrane-bound GLUT4 levels in skeletal muscle. These results suggest that AM plays a protective role in hyperglycemia-induced glycogen accumulation and cardiac and renal dysfunction via Akt signal transduction pathways.