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We describe metabolically flexible Acidobacteriota MAGs that contain all genes to completely degrade Sphagnum cell wall sugars under both aerobic and anaerobic conditions. Finally, we propose a hypothetical model of acetate oxidation driven by changes in peat redox potential that explain how bogs may circumvent aceticlastic methanogenesis through aerobic and humics-driven respiration.The water-borne bacterium Legionella pneumophila is the causative agent of Legionnaires' disease. In the environment, the opportunistic pathogen colonizes different niches, including free-living protozoa and biofilms. The physiological state(s) of sessile Legionella in biofilms and their functional consequences are not well understood. Using single-cell techniques and fluorescent growth rate probes as well as promoter reporters, we show here that sessile L. pneumophila exhibits phenotypic heterogeneity and adopts growing and nongrowing ("dormant") states in biofilms and microcolonies. Phenotypic heterogeneity is controlled by the Legionella quorum sensing (Lqs) system, the transcription factor LvbR, and the temperature. The Lqs system and LvbR determine the ratio between growing and nongrowing sessile subpopulations, as well as the frequency of growth resumption ("resuscitation") and microcolony formation of individual bacteria. Nongrowing L. pneumophila cells are metabolically active, express virulence genes and show tolerance toward antibiotics. Therefore, these sessile nongrowers are persisters. Taken together, the Lqs system, LvbR and the temperature control the phenotypic heterogeneity of sessile L. pneumophila, and these factors regulate the formation of a distinct subpopulation of nongrowing, antibiotic tolerant, virulent persisters. Hence, the biofilm niche of L. pneumophila has a profound impact on the ecology and virulence of this opportunistic pathogen.<br />To determine the effect of vasopressin on arterial blood pressure in infants with neonatal hypertrophic obstructive cardiomyopathy (HOCM).<br />Retrospective case study in Neonatal ICU involving six infants; five born to mothers with diabetes mellitus (mean gestational age 37.5 ± 0.9 weeks). Vasopressin infusion was started at a mean dose of 0.3 ± 0.2 mU/kg/min.<br />Initiation of vasopressin was followed by improved mean (p = 0.004), systolic (p = 0.028), and diastolic (p = 0.009) arterial pressure within 2 h. Heart rate (p = 0.025) and oxygen requirement (p = 0.021) also declined after initiation. Serum sodium declined initially and recovered by 72 h (p = 0.017).<br />Although there is limited experience with vasopressin use in neonatal HOCM, our case series suggests it may be beneficial for improving systemic hypotension and stabilization of hemodynamics. The potential for hyponatremia is high, necessitating careful fluid/electrolyte management. A prospective randomized trial is necessary to confirm safety and efficacy of vasopressin treatment in neonatal HOCM.<br />Although there is limited experience with vasopressin use in neonatal HOCM, our case series suggests it may be beneficial for improving systemic hypotension and stabilization of hemodynamics. The potential for hyponatremia is high, necessitating careful fluid/electrolyte management. A prospective randomized trial is necessary to confirm safety and efficacy of vasopressin treatment in neonatal HOCM.<br />Diet plays a key role in the ageing process. Despite this, little is known about the effect of dietary patterns on older adults' nutritional status. The main aim of this study was to analyse the association between a posteriori derived dietary patterns (DPs) and nutritional status among community dwellers aged ≥65.<br />Cross-sectional study including a representative sample of the community-dwelling Portuguese population aged ≥65 (n = 849, mean age 74.1 years old). Data were collected through computer-assisted, face-to-face interviews. Dietary patterns were derived a posteriori based on two 24-h recalls by a latent class transition model. #link# Nutritional status was assessed by the Mini Nutritional Assessment (MNA<br />) and measured body mass index (BMI). link2 Associations were estimated by regression models. MNA score was reversed and log-transformed considering its skewed distribution.<br />Two DPs were identified 22.0% of the studied population followed a 'Protein-based foods' DP (highest consumption of legumes, meats and sweets), and 59.1% followed a 'Mediterranean' DP (highest consumption of vegetables, fruits, dairy, cereals/tubers, bread, fishery and olive oil). Moreover, 18.9% switched between those patterns ('In-between' DP). After adjustment, the 'Protein-based foods' DP was associated with better MNA score (EXP(β) = 0.716, 95% CI 0.533, 0.962), compared to the 'Mediterranean' DP, particularly for total energy intake up to 2200 kcal/day. No significant associations were found between DPs and BMI.<br />A protein-based pattern is associated with lower malnutrition risk in older adults, when considering an adequate energy intake. This should be taken into account when designing and disseminating food-based guidelines for healthy ageing.<br />A protein-based pattern is associated with lower malnutrition risk in older adults, when considering an adequate energy intake. This should be taken into account when designing and disseminating food-based guidelines for healthy ageing.Cells are minimal functional units in biological phenomena, and therefore single-cell analysis is needed to understand the molecular behavior leading to cellular function in organisms. In addition, omics analysis technology can be used to identify essential molecular mechanisms in an unbiased manner. Recently, single-cell genomics has unveiled hidden molecular systems leading to disease pathogenesis in patients. In this review, I summarize the recent advances in single-cell genomics for the understanding of disease pathogenesis and discuss future perspectives.Gastric cancer (GC) is one of the most leading malignancies. Long noncoding RNA is related to GC. In this study, 11 miRNAs in the exosomes and six lncRNAs in the tissues was examined by qRT-PCR. Correlation analysis was used to analyze the relationship between miRNAs in exosome and lncRNAs in the tissues. [https://www.selleckchem.com/products/ldk378.html Ceritinib] in GC tissues were examined by qRT-PCR. MTT was used to determine cell viability. Flow cytometry was used to quantify the apoptotic cells. Transwell assay was used to examine the migration and invasion capacity. Dual-luciferase assay was used to examine the interaction between HOTAIR and miR-30a or -b. Capillary formation was used to determine the capillary formation capacity. Weak negative correlations were found between HOTAIR and miR-30a or -b in GC tissue samples. Interestingly, strong negative correlations were identified between the HOTAIR level in GC tissue samples and the miR-30a or -b levels in plasma exosomes. HOTAIR knockdown GC cells exhibited decreased migration, invasion, proliferation, and upregulated apoptosis, which released more miR-30a and -b into the exosomes. KRAS was upregulated when co-cultured with exosomes from HOTAIR overexpressed cells, and promoted GC cells proliferation, migration, and invasion. Meanwhile, HUVEC cells expressed increased VEGF-A and formatted more capillaries. Subsequently, we identified a 10mer target site of miR-30a or -b in HOTAIR sequence, and the overexpression of HOTAIR induced the degradation of miR-30a or -b, indicating a ceRNA role of HOTAIR. We report the negative correlation between the plasma miRNAs level and GC tissue HOTAIR expression for the first time and unveiled the ceRNA role of HOTAIR in GC. HOTAIR functions as an onco-lncRNA regulating the level of miR-30a and -b in both GC cells and exosomes. These findings may give insight into understanding the mechanism of GC pathogenesis and provide new biomarkers for clinical diagnosis.<br />The hypothalamo-pituitary-adrenal (HPA) axis is perturbed in obesity. We previously reported presence of leptin resistance in the brainstem and uncoupling between central noradrenergic tone and the HPA axis in obesity-prone (DIO) rats. link3 Metformin is shown to lower body weight and adiposity, but the underlying mechanism is unclear. We hypothesized that this is associated with restored HPA axis function.<br />Adult male DIO rats were placed on either a regular chow or HF diet for 7 weeks. Starting week 4, the animals were given either a low dose (60 mg/kg) or high dose (300 mg/kg) of metformin in drinking water. In addition to body weight and feeding, we examined different arms of the HPA axis to test if metformin can reinstate its function and coupling. To understand potential mechanisms, leptin signaling in the brainstem and circulating free fatty acid levels were also assessed.<br />Metformin treatment lowered weight gain, fat mass, caloric intake, and serum leptin levels. HPA axis activity as determined by corticotropin-releasing hormone in the median eminence and serum corticosterone was decreased by metformin in a dose-dependent manner, and so was norepinephrine (NE) in the paraventricular nucleus. Importantly, metformin completely normalized the NE-HPA axis uncoupling. While brainstem pSTAT-3 and SOCS-3, key markers of leptin signaling, were not different between groups, circulating saturated and unsaturated free fatty acids were reduced in HF-fed, metformin-treated animals.<br />These findings suggest that oral metformin can successfully correct HPA axis dysfunction that is associated with lowered circulating free fatty acids in DIO rats, thereby uncovering a novel effect of metformin in the treatment of obesity.<br />These findings suggest that oral metformin can successfully correct HPA axis dysfunction that is associated with lowered circulating free fatty acids in DIO rats, thereby uncovering a novel effect of metformin in the treatment of obesity.Foxp1 is a tumor suppressor in colon cancer. However, circFoxp1 derived from Foxp1 is an oncogene. In this study, we aim to investigate the role of circFoxp1 in colon cancer and the regulatory mechanism between circFoxp1 and Foxp1. 78 human colon tumor tissues and the matched paracancerous tissues were collected. Quantitative polymerase chain reaction, immunohistochemistry, quantitative methylation-specific PCR, chromatin immunoprecipitation assay, CCK-8 assay, and Tumor xenograft in nude mice were performed. The expression of circFoxp1 was increased and Foxp1 was reduced in colon cancer tissues, which were associated with a poor overall survival rate of the patients with colon cancer. CircFoxp1 recruited DNMT1 to the promoter of Foxp1, leading to promotor hypermethylation, thereby inhibiting Foxp1 transcription. Interfering circFoxp1 by siRNA in SW620 cells significantly inhibited cell viability, while knockdown Foxp1 expression partially restored SW620 cell viability. In addition, knockdown of circFoxp1 significantly sensitized colon cancer cells to Capecitabine in vitro and vivo through regulating Foxp1. We discovered a novel epigenetic pathway that circFoxp1 regulated Foxp1 in colon cancer cells. CircFoxp1 may regulate DNA methylation and demethylation to coordinate colon cancer cell proliferation and participate in chemotherapy drug responses. Therefore, circFoxp1 may be a potential therapeutic target for colon cancer.