The Interrater and Intrarater Reliability of the Humeral Head Ossification System and the Proximal Femur Maturity Index Assessments for Patients with Adolescent Idiopathic Scoliosis.

Background: Skeletal maturity can evaluate the growth and development potential of children and provide a guide for the management of adolescent idiopathic scoliosis (AIS). Recent studies have demonstrated the advantages of the Humeral Head Ossification System (HHOS) and the Proximal Femur Maturity Index (PFMI), based on standard scoliosis films, in the management of AIS patients. We further assessed the HHOS and the PFMI method's reliability in the interrater and intrarater. Methods: The data from 38 patients, including the humeral head and proximal femur on standard scoliosis films, were distributed to the eight raters in the form of a PowerPoint presentation. On 38 independent standard spine radiographs, raters utilized the HHOS and PFMI to assign grades. The PPT sequence was randomly changed and then reevaluated 2 weeks later. For every system, the 95% confidence interval (95% CI) and intraclass correlation coefficient (ICC) were calculated to evaluate the interrater and intrarater reliability. Results: The HHOS was extremely reliable, with an intraobserver ICC of 0.802. In the first round, the interobserver ICC reliability for the HHOS was 0.955 (0.929-0.974), while in the second round, it was 0.939 (0.905-0.964). The PFMI was extremely reliable, with an intraobserver ICC of 0.888. In the first round, the interobserver ICC reliability for the PFMI was 0.967 (0.948-0.981), while in the second round, it was 0.973 (0.957-0.984). Conclusions: The HHOS and PFMI classifications had excellent reliability. These two methods are beneficial to reduce additional exposure to radiation and expense for AIS. There are advantages and disadvantages to each classification. Clinicians should choose a personalized and reasonable method to assess skeletal maturity, which will assist in the management of adolescent scoliosis patients.

Isolation, characterization and transcriptome analysis of porcine deltacoronavirus strain HNZK-02 from Henan Province, China.

Porcine deltacoronavirus (PDCoV), an emerging porcine enteropathogenic coronavirus, causes acute watery diarrhea and vomiting in piglets. Here, we isolated a strain of PDCoV from intestinal content of a piglet with severe watery diarrhea on a farm located in Henan Province, named PDCoV strain HNZK-02. Subsequently, the complete genomes of cell-cultured PDCoV HNZK-02 passage 5 and 15 were sequenced and analyzed. There was a continuous 3-nucleotide deletion and 7 amino acid changes in S genes when compared with the other reported PDCoVs. RNA sequencing (RNA-seq)-based transcriptome analysis was used to quantitatively identify differentially expressed genes after PDCoV infection in ST cells. In total, 523 differentially expressed genes (DEGs) were identified, including 62 upregulated genes and 457 downregulated genes. The 62 upregulated genes were associated with TNF signaling pathway, cytokine-cytokine receptor interaction, Toll-like receptor signaling pathway, IL-17 signaling, chemokine signaling pathway and NF-κB signaling pathway. The significant expressing changed genes, including three antiviral genes (Mx1, OASL, OAS1) and three inflammatory chemokine related genes (CCL5, CXCL8, CXCL10) were further validated using quantitative real-time RT-PCR (qRT-PCR) assay. It showed the consistent expression patterns of the candidate genes with those from RNA-seq. Our results demonstrated that PDCoV infection activates NF-κB signaling pathway and leads to the expression of inflammatory factors, which may be related to TLRs but TLR2 is not a critical factor.In general, these results can help us to confirm the molecular regulation mechanism and also provide us a comprehensive resource of PDCoV infection.

Porcine deltacoronavirus infection alters bacterial communities in the colon and feces of neonatal piglets.

Porcine deltacoronavirus (PDCoV) is a novel enteropathogenic coronavirus that causes watery diarrhea in piglets. Little is known regarding the alteration of the gut microbiota in PDCoV-induced diarrhea piglets. In this study, 5-day-old piglets were experimentally infected with PDCoV strain CH-01, and all piglets developed typical clinical disease, characterized by acute and severe watery diarrhea. Histologic lesions were limited to the villous epithelium of the duodenum and ileum. Gut microbiota profiles in the colon and feces of piglets inoculated with PDCoV were investigated using 16S rRNA sequencing. The results showed that PDCoV infection reduced bacterial diversity and significantly altered the composition of the microbiota from the phylum to the genus level in the colon and feces of piglets. Firmicutes (phylum), Lactobacillaceae (family), and Lactobacillus (genus) were significantly increased (p < .01), while the abundance of Bacteroidetes (phylum) was markedly reduced in the colon and feces of the PDCoV-infected piglets (p < .01) when compared to those of the healthy piglets. Furthermore, microbial function prediction indicated that the changes in the intestinal flora also affected the nucleotide transport and metabolism, defense, translation, and transcription function of the intestinal microbiota. The current study provides new insight into the pathology and physiology of PDCoV.

A nano silicon adjuvant enhances inactivated transmissible gastroenteritis vaccine through activation the Toll-like receptors and promotes humoral and cellular immune responses.

Inactivated transmissible gastroenteritis virus (TGEV) vaccines are widely used in swine herds in China. These are limited, however, by the need to elicit both humoral and cellular immunity, as well as the efficiency of adjuvants. In this study, a 70-nm nano silicon particle was applied with inactivated TGEV vaccine in mice, and its immune-enhancing effects and mechanism of action investigated. We found that nano silicon applied with inactivated TGEV vaccine induced high antibody titers, increase IL-6, TNF-α and IFN-γ expression, and stimulate CD3+ T cell proliferation with a high CD4+/CD8+ T lymphocyte ratio. Nano silicon could quickly activate innate and adaptive immunity by stimulating Toll-like receptor signaling pathways, indicating that the nano silicon adjuvant enhanced long-term humoral and early cellular immune responses when combined with inactivated TGEV vaccine. Nano silicon could be considered for use as an antigen- carrier and adjuvant for veterinary vaccines.

Porcine parvovirus infection activates inflammatory cytokine production through Toll-like receptor 9 and NF-κB signaling pathways in porcine kidney cells.

Porcine parvovirus virus (PPV) is an animal virus that has caused high economic losses for the swine industry worldwide. Previous studies demonstrated that PPV infection induced significant production of interleukin 6 (IL-6) in vitro and in vivo. However, the inflammatory cytokines and specific signaling pathways induced during PPV infection remain largely unknown. In the present study, we analyzed the expression levels of IL-6 in PPV-infected porcine kidney 15 (PK-15) and the results showed that PPV infection induced the increase of IL-6 mRNA expression in a dose-dependent manner. We also detected the expression of toll-like receptor 9 (TLR9) signaling proteins in the mRNA expressing level, when compared with the control group, the TLR9 expression in mRNA level increased at 24h in PK-15 cells after PPV infection and reached the peak level at 48h. In addition, the transcript profile of nuclear factor kappa B (NF-κB) signal pathway relating genes (MyD88, IRAK1, TRAF6, TAK1α, IκBκB and NF-κB) expression levels increased at different times. Furthermore, to verify the IL-6 expression was specific with the TLR9 expression and then by activating the NF-κB signal pathway, TLR9 and NF-κB specific inhibitors were applied during PPV infection, separately, the result indicated that the expression of IL-6 was decreased after inhibitor treatment. Taken together, PPV infection significantly induced IL-6 expression and this induction depended on NF-κB activation and TLR9 signaling pathways in PK-15 cell.