Association of Self-Reported Nighttime Sleep Duration with Chronic Kidney Disease: China Health and Retirement Longitudinal Study.

INTRODUCTION: The cohort study aimed to assess the association of nighttime sleep duration and the change in nighttime sleep duration with chronic kidney disease (CKD) and whether the association between nighttime sleep duration and CKD differed by daytime napping. METHODS: This study included 11,677 individuals from the China Health and Retirement Longitudinal Study (CHARLS) and used data from the 2011 baseline survey and four follow-up waves. Nighttime sleep duration was divided into three groups: short (<7 h per night), optimal (7-9 h), and long nighttime sleep duration (>9 h). Daytime napping was divided into two groups: no nap and with a nap. We used Cox proportional hazards model to examine the effect of nighttime sleep duration at baseline and change in nighttime sleep duration on incident CKD and a joint effect of nighttime sleep duration and nap time on onset CKD. RESULTS: With a follow-up of 7 years, the incidence of CKD among those with short, optimal, and long nighttime sleep duration was 9.89, 6.75, and 9.05 per 1,000 person-years, respectively. Compared to individuals with optimal nighttime sleep duration, short nighttime sleepers had a 44% higher risk of onset CKD (hazard ratio [HR]: 1.44, 95% confidence interval [CI]: 1.21-1.72). Compared to participants with persistent optimal nighttime sleep duration, those with persistent short or long nighttime sleep duration had an increased risk of incident CKD (HR: 1.44, 95% CI: 1.15-1.80). We found a lower incidence of CKD in participants with short nighttime sleep duration and a nap (HR: 0.74, 95% CI: 0.60-0.93), compared to those with short nighttime sleep duration and no nap. CONCLUSION: Short nighttime sleep duration and persistent long or short nighttime sleep duration were associated with a higher risk of onset CKD. Keeping persistent optimal nighttime sleep duration may help reduce CKD risk later in life. Daytime napping may be protective against CKD incidence.

MoRts1, a regulatory subunit of PP2A, is required for fungal development and pathogenicity of Magnaporthe oryzae.

Protein phosphatase 2 A (PP2A) is a major heterotrimeric serine/threonine protein phosphatase comprised of three subunits, including structural subunits (A), regulatory subunits (B), and catalytic subunits (C). PP2A has been widely shown to involve in a series of cell signal transduction processes such as cell metabolism, cell cycle regulation, DNA replication, gene transcription and protein translation in yeast and mammalian. However, the roles of PP2A in pathogenic fungi Magnaporthe oryzae still remain unclear. We here found that MoRts1, a gene encoding B regulatory subunit of PP2A homologous to Saccharomyces cerevisiae Rts1, showed up-regulated transcription during conidia and initially infectious stage. Subcellular localization revealed that MoRts1-eGFP was localized to the cytoplasm and septum. Targeted disruption of MoRts1 leads to a reduction of mycelial growth and sporulation, as well as the defects of hydrophobicity, melanin pigmentation and cell wall integrity (CWI). The MoRts1 mutants were less pathogenic to the host plants, compared to the Ku80 strain, and the transcriptional levels of several pathogenicity-related Rho GTPase genes, including MoCdc42, MoRho2, MoRho3, MoRho4, MoRhoX and MoRac1, were significantly decreased in the MoRts1 mutants. Besides, two splicing variants of MoRts1 with unique functions of regulating the growth and pathogenicity were identified, and the B56 domain is vital for determining the sporulation and pathogenicity of M. oryzae. Furthermore, MoRts1 was identified to interact with PP2A catalytic subunit MoPPG1 in vivo in M. oryzae. In summary, our results showed that MoRts1 is an important regulator contributing to the fungal development, and pathogenicity of M. oryzae.

Graft-versus-host disease complicated with small bowel obstruction in children: A case report.

Graft-versus-host disease (GvHD) is a severe complication following hematopoietic cell transplantation (HCT). The clinical manifestations of GvHD can affect multiple systems. Although gastrointestinal (GI) GvHD is common, GI obstruction complications are rare. Here, we present a case of GI-GvHD after HCT for acute myeloid leukemia (AML) in a young girl from China. The patient suffered from watery diarrhea, which progressed to bloody diarrhea 40 days after HCT. She experienced prolonged and repeated mucous or bloody stool after the withdrawal of cyclosporine and the gradual reduction in methylprednisolone. The plain abdominal radiography and computed tomographic (CT) scan showed apparent bowel wall thickening and intestinal stenosis 10 months after HCT. Finally, the patient underwent surgery to remove the small intestinal stenosis at the age of 26 months. The patient recovered with the help of appropriate medical therapies and nutritional support during hospitalization. She remained stable, and there was no recurrence of GI symptoms 16 months after the surgery. In summary, surgery may be an optimal treatment for GvHD patients with persistent bowel obstruction and failure of appropriate immunosuppressive therapies.

Functional characterization of MoSdhB in conferring resistance to pydiflumetofen in blast fungus Magnaporthe oryzae.

BACKGROUND: Rice (Oryza sativa) is an important cereal crop around the world, and has constantly been threaten by the most destructive fungus Magnaporthe oryzae. Pydiflumetofen, a novel succinate dehydrogenase inhibitor (SDHI), is currently being used for controlling various fungal diseases. However, the potential resistance risk of M. oryzae to pydiflumetofen has remained unclear to date, and finding the resistance mechanism is critical for the usage of this fungicide. RESULTS: The M. oryzae strain Guy11 is sensitive to pydiflumetofen, with EC50 value of 1.24 µg mL-1 . 58 pydiflumetofen-resistant (PR) mutants were obtained through pydiflumetofen-induced spontaneous mutation, with a mean EC50 value >500 µg mL -1 , and the resistance factor (RF) >400. The PR mutants displayed positive cross-resistance to carboxin, but were more sensitive to fluopyram. Sequencing analysis showed that all PR mutants presented a cytosine-to-thymine transition at nucleotide position +1218, resulting in a replacement of histidine 245 by tyrosine (H245Y) on MoSdhB. The mutation of MoSdhB exhibited strong resistant phenotype, but no detectable growth deficits in fungal development, including vegetative growth and pathogenicity of M. oryzae. An allele-specific PCR for rapid detection of the H245Y mutants was established in M. oryzae. CONCLUSION: The M. oryzae is sensitive to pydiflumetofen, and shows a medium to high resistance risk to pydiflumetofen. A point mutation of MoSdhB (H245Y) is responsible for the fungal resistance to pydiflumetofen in M. oryzae. © 2022 Society of Chemical Industry.

Recanalization of symptomatic chronic internal carotid artery occlusions by hybrid treatment.

OBJECTIVE: To evaluate the efficacy and safety of hybrid revascularization by carotid endarterectomy and endovascular intervention in the treatment of chronic internal carotid artery occlusion (ICAO). METHODS: We performed a retrospective analysis of patients who received hybrid treatment for symptomatic chronic ICAO between December 2016 and December 2018. Fifty-six patients with long-segment ICAO were enrolled and divided into the short duration (1-3 months) and long ICAO duration (>3 months) groups, and their clinical and angiographic data were analyzed. RESULTS: The mean duration was 106.8 ± 36.1 days from the date of ICAO diagnosis to revascularization. Totally, 10 patients (17.8%, n = 56) in the short duration group while no patients in the long duration group failed recanalization (n = 7). Perioperative complications included intraoperative thromboembolism in 1 (1.8%) patient and subarachnoid hemorrhage in 2 (3.6%) patients. Early phase postoperative hypertension was noted in 11 (19.6%) patients and cervical hemorrhage in 1 (1.8%) patient. No severe neurological deficits occurred. Overall, the 6-month modified Rankin score, Mini-mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA) scores in patients with successful recanalization significantly improved versus the baseline (P < 0.05). After successful recanalization, the long duration group demonstrated more stents for revascularization compared with the short duration group (P < 0.05). Five (10.8%) patients had recurrent transient ischemic attack, and 1 (2.2%) patient developed stroke in the successful revascularization group during 6 months of follow-up. ICA restenosis occurred in 5 (8.9%) patients and re-occlusion was noted in 1 (1.8%) patient. CONCLUSIONS: Hybrid operation may be feasible and effective for patients with symptomatic chronic complete ICAO according to our limited data. The original occlusion site from the carotid bifurcation and the duration of ICAO should be considered as independent indicators for successful recanalization as well as perioperative outcomes.

Case Report: Pediatric Recurrent Acute Liver Failure Caused by Neuroblastoma Amplified Sequence (NBAS) Gene Mutations.

Acute liver failure (ALF) in childhood is a rapidly progressive, potentially life-threatening condition that occurs in previously healthy children of all ages. However, the etiology of ~50% of cases with pediatric ALF remains unknown. We herein report a 4-year-old Chinese girl with recurrent ALF (RALF) due to a mutation in the neuroblastoma amplified sequence (NBAS) gene. The patient had suffered from multiple episodes of fever-related ALF since early childhood. She had also suffered from acute kidney injury, hypertension, mild pulmonary hypertension, pleural effusion, and hypothyroidism. A novel compound heterozygote mutation, c.3596G> A (p.C1199Y)/ex.9del (p.216-248del), in the NBAS gene was identified by whole-exome sequencing (WES). The missense mutation c.3596G> A (p. C1199Y) was inherited from her father, and ex.9del (p.216-248del) was inherited from her mother. The patient was managed with intensive treatments, such as renal replacement therapy (CRRT), intravenous antibiotics, and glucose infusion, and was discharged after full recovery. We identified a novel compound heterozygote mutation in the NBAS gene that caused fever-related RALF in a Chinese child, which further expands the mutational spectrum of NBAS.