Genome Sequence Resource for Colletotrichum viniferum, the Cause of Grapevine Ripe Rot in China.

Grape ripe rot is an important disease that has seriously damaged the yield and quality of grape worldwide. The disease is caused by Colletotrichum viniferum, a hemibiotrophic fungus that belongs to the Glomerellaceae family of Sordariomycetes class. Here, we present the genome of C. viniferum CvYL2a from grape, based on Illumina HiSeq 2500 and PacBio RS II. The high-quality genome consists of 70 contigs with a 73.41 Mb genome size and encodes 14,668 protein-coding genes. These genes were annotated using Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, EuKaryotic Orthologous Groups, Nonredundant Protein, and Swiss-Prot databases. In addition, we identified a series of genes involved in pathogenicity, including 909 carbohydrate-active enzymes, 67 secondary metabolite gene clusters, and 307 cytochrome P450 enzymes. This genome sequence provides a valuable reference for research on grape-C. viniferum interactions, the pathogenesis of C. viniferum, and comparative genome analyses.[Formula: see text] Copyright © 2021 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.

The prevalence and clinical presentation of Hirschsprung's disease in preterm infants: a systematic review and meta-analysis.

PURPOSE: Hirschsprung's disease (HD) is a rare occurrence in premature infants, and the exact prevalence varying across studies. Thus, we conducted this study to determine the prevalence of and clinical presentation of HD in preterm infants. METHODS: The PubMed, EmBase, and Cochrane library databases were searched for eligible studies throughout May 2021. The pooled incidence with 95% confidence interval (CI) was calculated using the random-effects model. RESULTS: Thirty studies involved 4,557 children with HD were included. The pooled proportion of HD patients who were preterm infants was 7% (95% CI 5-8%; P < 0.001); the sensitivity analysis indicated that the pooled prevalence of preterm infants with HD ranged from 5.0% to 5.6%. Moreover, the pooled incidence of abdominal distention in HD patients was 83% (P < 0.001), that of vomiting was 61% (P < 0.001), that of bilious vomiting was 54% (P < 0.001), that of delayed meconium passage was 48% (P < 0.001), that of constipation was 44% (P < 0.001), and that of enterocolitis was 13% (P < 0.001). CONCLUSIONS: This study reported the prevalence of HD patients who were preterm infants, and the most common presentations were abdominal distention, vomiting, bilious vomiting, delayed meconium passage, constipation, and enterocolitis.

Association of neural tube defects with congenital abnormalities of the urogenital system in a Chinese cohort.

BACKGROUND: This study aimed to retrospectively analyze the correlation between congenital abnormality of the urogenital system and various factors in children with neural tube defects (NTDs). METHODS: A total of 190 children with congenital NTDs, who were admitted to a hospital from May 2013 to May 2018, were included into the present study. All admitted children with congenital NTDs were carried out routine abdominal B-ultrasound examinations to determine the malformations of the abdominal organs, including the urinary system. Children with a B-ultrasound result of suspected and unsure malformation underwent intravenous pyelography (IVP) and voiding cysto-urethrography (VCU), and this was further confirmed by the CT results. RESULTS: The incidence of urogenital malformation was 12.1% (23/190) in children with congenital NTDs. For the 23 children with urogenital malformations, most of these children had no definite urinary system symptoms, while some of these children had multiple incidences of urinary system infections. CONCLUSIONS: Congenital NTDs are often combined with urogenital malformations, if not specifically searched these may be overlooked. The early detection of these malformations is beneficial to reduce the risk of operation and improve the prognosis.

Norcantharidin inhibits lymphangiogenesis by downregulating the expression of VEGF-C and VEGF-D in human dermal lymphatic endothelial cells in vitro.

AIMS: To investigate the effects of norcantharidin on the growth and migration of human dermal lymphatic endothelial cells (HDLECs) and further characterize its effect on lymphangiogenesis. METHODS: A 3-dimensional fibrin gel lymphangiogenesis model was built. Flow cytometry was used to analyze the rate of apoptosis and necrosis. RT-PCR, immunohistochemistry and immunoblotting assays were used to examine the effect of norcantharidin on vascular endothelial growth factor C (VEGF-C), VEGF-D and VEGF receptor 3 during in vitro lymphangiogenesis. RESULTS: Norcantharidin caused a marked dose and time-dependent inhibition of the growth of HDLECs with an IC50 of 40 nmol/l. The apoptotic rate of HDLECs was 13.21 ± 1.60% 24 h after treatment with 7.5 nmol/l norcantharidin and 42.34 ± 3.80% with 90 nmol/l norcantharidin (p < 0.01 vs. controls in both). Fibrin gel assays showed that norcantharidin (15 nmol/l) reduced the number of tubular structures from 68.4 ± 5.2 in untreated controls to 10.9 ± 2.3 (p = 0.000). RT-PCR, immunohistochemistry and immunoblotting assays showed norcantharidin markedly reduced the expression of VEGF-C and VEGF-D. CONCLUSION: Norcantharidin inhibits lymphangiogenesis by downregulating the expression of VEGF-C and VEGF-D, suggesting that norcantharidin could be an effective agent for targeting neolymphangiogenesis.

Circulating exosomal microRNA-18a-5p accentuates intestinal inflammation in Hirschsprung-associated enterocolitis by targeting RORA.

The relevance of stem cell-derived exosomes has been implicated in necrotizing enterocolitis, while the involvement of serum-derived exosomes from children with Hirschsprung-associated enterocolitis (HAEC) in pathogenesis of HAEC remains unclear. This study set to identify the roles of exosomal microRNA (miR)-18a-5p from sera of HAEC patients in human-derived colonic epithelial NCM460 cells and in mice with HAEC. Exosomes were isolated from the sera of healthy children (Healthy-exo), patients with Hirschsprung's disease (HSCR) (HSCR-exo) or HAEC (HAEC-exo). A microarray analysis of miRNAs was implemented to assess the enrichment of miRNAs in these exosomes. HAEC-exo was significantly enriched in miR-18a-5p. HAEC-exo led to the generation of a pro-inflammatory microenvironment, inhibition of cellular DNA synthesis, and promotion of apoptosis in NCM460 cells. Mechanistically, miR-18a-5p targeted and repressed retinoid-related orphan receptor α (RORA) expression, thereby regulating the Sirtuin 1 (SIRT1)/nuclear factor-kappa B (NFκB) pathway. Overexpression of RORA ameliorated inflammatory damage in NCM460 cells caused by exosomal miR-18a-5p. HAEC-exo exacerbated inflammatory damage in HAEC mice, and this facilitation was reversed after RORA overexpression. Collectively, exosomal miR-18a-5p was a promoter of HAEC, which induces the intestine cell apoptosis and inflammatory responses through the inhibition of SIRT1/NFκB pathway by targeting RORA.

Influences of Experience and Visual Cues of Virtual Arm on Distance Perception.

Egocentric distance perception refers to the perception of distance from a target to a perceiver, which is an important component of visual space perception. It is important to activities in virtual environments and influenced by several factors, such as action capacities and visual cues. However, few studies have investigated such aspects. Hence, Experiments 1 and 2 investigated the effect of using experience and visual cues, respectively, of virtual arms on egocentric distance perception in near and far spaces at equal, prolonged, and shortened lengths of a virtual arm. Results revealed that using experience and visual cues of the virtual arm had a significant effect on egocentric distance perception when the length of virtual arm was equal to the real arm and prolonged but not when shortened. The egocentric distance perception on the conditions of having using experience and virtual arm was most precise. The findings provide implications for the design and implementation of virtual body self-representation in virtual environments.

New model of in-situ xenograft lymphangiogenesis by a human colonic adenocarcinoma cell line in nude mice.

OBJECTIVE: To explore a new model of in-situ xenograft lymphangiogenesis of human colonic adenocarcinomas in nude mice. METHOD: On the basis of establishing subcutaneous xenograft lymphangiogenesis model of human colonic adenocarcinoms, in-situ xenografts were established through the in situ growth of the HT-29 human colonic adenocarcinoma cell line in nude mice. The numbers of lymphangiogenic microvessels, the expression of lymphatic endothelial cell markers lymphatic vessel endothelial hyaloronic acid receptor-1 (LYVE-1), D2-40 and the lymphatic endothelial growth factors vascular endothelial growth factor-C (VEGF-C), -D (VEGF-D) and receptor-3 (VEGFR-3) were compared by immunohistochemical staining, Western bolt and quantitative RT-PCR in xenograft in-situ models. RESULTS: Some microlymphatics with thin walls, large and irregular or collapsed cavities and increased LMVD, with strong positive of LYVE-1, D2-40 in immunohistochemistry, were observed, identical with the morphological characteristics of lymphatic vessels and capillaries. Expression of LYVE-1 and D2-40 proteins and mRNAs were significantly higher in xenografts in-situ than in the negative control group (both P<0.01). Moreover, the expression of VEGF-C, VEGF-D and VEGFR-3 proteins and mRNAs were significantly higher in xenografts in-situ (both P<0.01), in conformity with the signal regulation of the VEGF-C,-D/VEGFR-3 axis of tumor lymphangiogenesis. CONCLUSIONS: In-situ xenografts of a human colonic adenocarcinoma cell line demonstrate tumor lymphangiogenesis. This novel in-situ animal model should be useful for further studying mechanisms of lymph node metastasis, drug intervention and anti-metastasis therapy in colorectal cancer.

Suppression of lymphangiogenesis in human lymphatic endothelial cells by simultaneously blocking VEGF-C and VEGF-D/VEGFR-3 with norcantharidin.

Lymph node metastasis of tumors is a crucial early step in the metastatic process. Tumor lymphangiogenesis plays an important role in promoting tumor metastasis to regional lymph nodes. Norcantharidin (NCTD) has been reported to possess potent anti-angiogenesis and antitumor properties in several cell lines and xenograft tumor models. However, its role in tumor-associated lymphangiogenesis and lymphatic metastasis remains unclear. Here, we investigated the effect of NCTD on proliferation, apoptosis, migration, invasion and the lymphatic tube formation, lymphangiogenesis, of human lymphatic endothelial cells (HLECs) in vitro by MTT, proliferation assay, Hoechst staining and flow cytometry, scraping line method, Matrigel invasion assay, inverted or fluorescence microscope and transmission electron microscope. Moreover, the underlying mechanisms, such as VEGF-C, VEGF-D, VEGFR-3 at protein and mRNA levels in lymphangiogenesis using 3-dimensional (3-D) culture of HLECs were measured by immunohistochemistry, western blotting and real-time polymerase chain reaction (RT-PCR). It was shown that NCTD inhibited proliferation, migration, invasion and lymphatic tube formation (forming-lymphatic and/or formed-lymphatic) of HLECs, induced HLEC apoptosis (all P<0.01) significantly, in a dose- and time-dependent manner (IC50 6.8 µg/ml); and downregulated the expression of VEGF-C, VEGF-D and VEGFR-3 at protein or/and mRNA levels (P<0.01) in HLEC lymphatic tube formation. Thus, we identified for the first time that NCTD inhibited HLEC lymphangiogenesis by simultaneously blocking VEGF-C and VEGF-D/VEGFR-3 in vitro. The present findings may be of importance to explore the therapeutical target or strategy of NCTD for tumor lymphangiogenesis and lymphatic metastasis.

Embedded-atom-method interatomic potentials from lattice inversion.

The present work develops a physically reliable procedure for building the embedded-atom-method (EAM) interatomic potentials for the metals with fcc, bcc and hcp structures. This is mainly based on Chen-Möbius lattice inversion (Chen et al 1997 Phys. Rev. E 55 R5) and first-principles calculations. Following Baskes (Baskes et al 2007 Phys. Rev. B 75 094113), this new version of the EAM eliminates all of the prior arbitrary choices in the determination of the atomic electron density and pair potential functions. Parameterizing the universal form deduced from the calculations within the density-functional scheme for homogeneous electron gas as the embedding function, the new-type EAM potentials for Cu, Fe and Ti metals have successfully been constructed by considering interatomic interactions up to the fifth neighbor, the third neighbor and the seventh neighbor, respectively. The predictions of elastic constants, structural energy difference, vacancy formation energy and migration energy, activation energy of vacancy diffusion, latent heat of melting and relative volume change on melting all satisfactorily agree with the experimental results available or first-principles calculations. The predicted surface energies for low-index crystal faces and the melting point are in agreement with the experimental data to the same extent as those calculated by other EAM-type potentials such as the FBD-EAM, 2NN MEAM and MS-EAM. In addition, the order among the predicted low-index surface energies is also consistent with the experimental information.