Pelvic infection caused by periodontitis: A case report

Oral bacteria in patients with periodontitis can disseminate into the bloodstream via broken oral epithelial cells, causing odontogenic maxillofacial infections, brain abscesses and endocarditis. However, pelvic infection caused by periodontitis is rare. The case of a 48-year-old woman with a long history of recurrent periodontal infections, who complained of abdominal distention and pain for 14 days after dental implantation, is reported here. Pelvic ultrasound and magnetic resonance imaging signaled multiple inflammatory encapsulated effusions in the posterior uterus, which were removed by laparoscopic surgery and tested with metagenomic next-generation sequencing (mNGS). Through mNGS, numerous oral pathogens, including Filifactor alocis, were identified in the pelvic effusions. The patient was subsequently diagnosed with a pelvic infection originating from periodontitis, and recovered after undergoing surgery and targeted antibacterial treatment. Thus, the possibility of extrabuccal complications in patients with a history of periodontitis or invasive oral procedures merits closer attention

Atypical KCNQ1/Kv7 channel function in a neonatal diabetes patient: Hypersecretion preceded the failure of pancreatic β-cells.

KCNQ1/Kv7, a low-voltage-gated K+ channel, regulates cardiac rhythm and glucose homeostasis. While KCNQ1 mutations are associated with long-QT syndrome and type2 diabetes, its function in human pancreatic cells remains controversial. We identified a homozygous KCNQ1 mutation (R397W) in an individual with permanent neonatal diabetes melitus (PNDM) without cardiovascular symptoms. To decipher the potential mechanism(s), we introduced the mutation into human embryonic stem cells and generated islet-like organoids (SC-islets) using CRISPR-mediated homology-repair. The mutation did not affect pancreatic differentiation, but affected channel function by increasing spike frequency and Ca2+ flux, leading to insulin hypersecretion. With prolonged culturing, the mutant islets decreased their secretion and gradually deteriorated, modeling a diabetic state, which accelerated by high glucose levels. The molecular basis was the downregulated expression of voltage-activated Ca2+ channels and oxidative phosphorylation. Our study provides a better understanding of the role of KCNQ1 in regulating insulin secretion and β-cell survival in hereditary diabetes pathology

Identification of long-lived and stable mRNAs in the aged seeds of wheat

Seed germination relies on preserving mRNA integrity in dry seeds. However, the quality of mRNA in aged wheat seeds is not well understood. Here, we investigated 20 wheat varieties for seed longevity using controlled deterioration treatment (CDT) and identified that Chinese Spring seeds exhibit moderate longevity. We observed correlations between seed viability and RNA integrity in the aleurone and embryo cells after aging-treatment. Nanopore sequencing of whole seeds from natural aging treatment (NAT) and CDT for 25 days identified 3,083 full-length transcripts. We performed RNA-seq transcriptome profiling to classify the tissue origin of these transcripts under eight aging treatments, revealing the presence of 2,064 overlapping long-lived mRNAs (LLRs) in the seed embryo and 2,130 in the aleurone layers. These LLRs corresponded to genes with detectable transcription levels and at least one full-length transcript in their coding sequence. Notably, degradation percentages of these mRNAs varied among seeds of different wheat varieties with similar ages. We predicted 21 most stable LLRs with high GC% content and short coding sequence length, among which only one LLR was seed-specifically expressed and belonged to the late-embryogenesis-abundant (LEA) protein family. RT-PCR confirmed the expression of the seven LLR fragments in the aleurone layer and embryo of Chinese Spring seeds. We found three of the most stable LLRs (LLR13, LLR15, and LLR20) identified in Chinese Spring were more stable in high longevity varieties than in short longevity varieties after aging, indicating their potential roles in seed longevity and germination.Fil: Liang, Wangzhuang. Sichuan Agricultural University; ChinaFil: Dong, Huixue. Sichuan Agricultural University; ChinaFil: Guo, Xiaojiang. Sichuan Agricultural University; ChinaFil: Rodríguez, María Verónica. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Fisiológicas y Ecológicas Vinculadas a la Agricultura. Universidad de Buenos Aires. Facultad de Agronomía. Instituto de Investigaciones Fisiológicas y Ecológicas Vinculadas a la Agricultura; Argentina. Universidad de Buenos Aires. Facultad de Agronomía. Departamento de Producción Vegetal; ArgentinaFil: Cheng, Mengping. Sichuan Agricultural University; ChinaFil: Li, Maolian. Sichuan Agricultural University; ChinaFil: Benech-Arnold, Roberto Luis. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Fisiológicas y Ecológicas Vinculadas a la Agricultura. Universidad de Buenos Aires. Facultad de Agronomía. Instituto de Investigaciones Fisiológicas y Ecológicas Vinculadas a la Agricultura; Argentina. Universidad de Buenos Aires. Facultad de Agronomía. Departamento de Producción Vegetal; ArgentinaFil: Pu, Zhien. Sichuan Agricultural University; ChinaFil: Wang, Jirui. Sichuan Agricultural University; Chin

Hdac4 Mutations Cause Diabetes And Induce Β‐Cell Foxo1 Nuclear Exclusion

Background Studying patients with rare Mendelian diabetes has uncovered molecular mechanisms regulating β‐cell pathophysiology. Previous studies have shown that Class IIa histone deacetylases (HDAC4, 5, 7, and 9) modulate mammalian pancreatic endocrine cell function and glucose homeostasis. Methods We performed exome sequencing in one adolescent nonautoimmune diabetic patient and detected one de novo predicted disease‐causing HDAC4 variant (p.His227Arg). We screened our pediatric diabetes cohort with unknown etiology using Sanger sequencing. In mouse pancreatic β‐cell lines (Min6 and SJ cells), we performed insulin secretion assay and quantitative RT‐PCR to measure the β‐cell function transfected with the detected HDAC4 variants and wild type. We carried out immunostaining and Western blot to investigate if the detected HDAC4 variants affect the cellular translocation and acetylation status of Forkhead box protein O1 (FoxO1) in the pancreatic β‐cells. Results We discovered three HDAC4 mutations (p.His227Arg, p.Asp234Asn, and p.Glu374Lys) in unrelated individuals who had nonautoimmune diabetes with various degrees of β‐cell loss. In mouse pancreatic β‐cell lines, we found that these three HDAC4 mutations decrease insulin secretion, down‐regulate β‐cell‐specific transcriptional factors, and cause nuclear exclusion of acetylated FoxO1. Conclusion Mutations in HDAC4 disrupt the deacetylation of FoxO1, subsequently decrease the β‐cell function including insulin secretion, resulting in diabetes.PubMedWoSScopu