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The continuous cropping of sugar beet can result in soil degradation and a decrease in the sugar beet yield and quality. However, the role of continuous sugar beet (Beta vulgaris L. var. saccharifera) cropping in shaping the structure and function of the rhizosphere microbial community remains poorly investigated. In this study, we comparatively investigated the impact of different numbers of years of continuous sugar beet cropping on structural and functional changes in the microbial community of the rhizosphere using high-throughput sequencing and bioinformatics analysis. We collected rhizosphere soils from fields continuously cropped for one-year (T1), five-year (T5), and thirty-year (T30) periods, as well as one bulk soil (T0), in the Xinjiang Uygur Autonomous Region. The results demonstrated that continuous sugar beet cropping resulted in a significant decline in the community diversity of soil bacterial and fungal populations from T1 to T5. With continuous change in the structure of the microbial community, the Shannon diversity and observed species were increased in T30. With an abundance of pathogenic microbes, including Acidobacteria, Alternaria, and Fusarium, that were highly enriched in T30, soil-borne diseases could be accelerated, deduced by functional predictions based on 16S rRNA genes. Continuous sugar beet cropping also led to significant declines in beneficial bacteria, including Actinobacteria, Pseudomonas spp., and Bacillus spp. In addition, we profiled and analyzed predictive metabolic characteristics (metabolism and detoxification). The abundance of phenolic acid decarboxylase involved in the phenolic acid degradation pathway was significantly lower in groups T5 and T30 than that in T0 and T1, which could result in the phenolic compounds becoming excessive in long-term continuous cropping soil. Our results provide a deeper understanding of the rhizosphere soil microbial community's response to continuous sugar beet cropping, which is important in evaluating the sustainability of this agricultural practice.

Short beak and dwarfism syndrome (SBDS) has been constantly breaking out in China since 2015. It is caused by a novel goose parvovirus-related virus (NGPV) and can severely restrict the growth of ducks. In this study, seven NGPV stains were isolated from different regions in China between 2015 and 2016. To better understand the correlation between NGPV and goose parvovirus (GPV), we conducted complete genome sequencing and a comprehensive analysis of the NGPV genome. The phylogenetic and alignment analysis showed that NGPV is a branch of GPV, sharing 92.2%-97.1% nucleotide identity with GPV. Compared with classical GPV, five consensus nucleotide mutations in all the seven NGPV isolates and two 14-nucleotide-pair deletions in six NGPV isolates were found in the inverted terminal repeats, twelve and eight synchronous amino acid changes were found in the replication protein and capsid protein of NGPV, respectively, which might be important for viral gene regulation, humoral immune responses, and host transfer. Notably, SDLY1602 was demonstrated a recombinant strain, with the potential major parent GPV vaccine strain 82-0321v and the minor parent GPV wild strain GDaGPV. This is the first report showing that the recombination between two classical GPV strains generated a NGPV strain circulating in nature. This study will advance our understanding of NGPV molecular biology and facilitate to elucidate the evolutionary characteristics of GPV.

The incidence of renal‐related adverse events (AEs) with canagliflozin in patients with type 2 diabetes mellitus from a pooled population of patients in 7 active‐ and placebo‐controlled trials (N = 5598) and in a 104‐week study vs glimepiride (N = 1450) was low and similar in canagliflozin and non‐canagliflozin groups. In the study vs glimepiride, canagliflozin was associated with an initial acute decrease in estimated glomerular filtration rate (eGFR) that attenuated over time, while eGFR declined progressively over 104 weeks with glimepiride. The incidence of renal‐related AEs with canagliflozin was generally stable over time, while the incidence with glimepiride increased over 104 weeks. In the present analysis, based on postmarketing reports from the US Food and Drug Administration Adverse Event Reporting System, a potential signal was identified for acute kidney injury with all approved sodium glucose co‐transporter 2 (SGLT2) inhibitors (ie, canagliflozin, dapagliflozin and empagliflozin). The early onset of acute kidney injury events with SGLT2 inhibitors in postmarketing reports probably reflects the acute changes in eGFR attibutable to the known renal haemodynamic effects of SGLT2 inhibition.

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To investigate the effects of sevoflurane on cognitive function in old Sprague-Dawley (SD) rats and the expression of insulin-like growth factor-1 (IGF-1) in CA1 region of hippocampus. Forty Sprague-Dawley rats of 12 months old were randomly divided into five groups: the normal control group; 1.5% sevoflurane I group (be tested after received 1.5% sevoflurane for 1 day); 1.5% sevoflurane II group (be tested after received 1.5% sevoflurane for 7 day); 3.0% sevoflurane I group (be tested after received 3.0% sevoflurane for 1 day) and 3.0% sevoflurane II group (be tested after received 3.0% sevoflurane for 7 day). All SD rats were received 1.5 or 3.0% sevoflurane in a special glass anesthesia box for 2 h respectively, except for the normal control group. Y-maze was used to test the ability of learning and memory after being received sevoflurane for 1 or 7 days at the same moment portion. The altered expression level of IGF-1 in the hippocampus was tested to compare its transcripts by RT-PCR analysis. The results showed that 3% sevoflurane induced the decline of cognitive function and significantly deceased the IGF-1 expression at mRNA levels at 1 day in the 3.0% sevoflurane I group when compared with the normal control group. However, there were no significant difference among the other groups when compared with normal control group. Therefore, administration of sevoflurane might temporally affect the ability of cognitive function of rats through suppressing the IGF-1 expression at mRNA levels in hippocampus.