Upregulation of ketone body (β-hydroxybutyrate, βHB) utilization has been documented in human end-stage heart failure (HF), but is unclear if this is due to intrinsic cardiac metabolic remodeling or a HF-related catabolic state. This study sought to evaluate the maximal ketone body utilization capacity and its determinants in controls and in patients with moderate HF and reduced ejection fraction (HFrEF). 19 HFrEF patients and 9 controls underwent sampling from the arterial circulation (A) and coronary sinus (CS) to measure transmyocardial extraction of energy-providing substrates and oxygen. In a separate experiment, measurements were performed 80-min after oral administration of 25 g of ketone ester (KE, (R)-3-hydroxybutyl(R)-3-hydroxybutyrate) drink in 11 HFrEF and 6 control subjects. There were no statistically significant differences in fasting substrate levels and fractional extractions between HF and controls. Administration of KE increased βHB by 12.9-fold, revealing an increased ability to utilizther studies are needed to determine whether exogenous ketones may have a potential therapeutic role.Most patients with severe obesity will present some lipid-lipoprotein abnormalities. The atherogenic dyslipidemia associated with severe obesity is characterized by elevated fasting and postprandial triglyceride levels, low high-density lipoprotein cholesterol concentrations, and increased proportion of small and dense low-density lipoproteins. Bariatric surgery has been proven safe and successful in terms of long-term weight loss and improvement in obesity co-existing metabolic conditions including lipid-lipoprotein abnormalities. Nevertheless, bariatric surgery procedures are not all equivalent. We conducted a comprehensive critical analysis of the literature related to severe obesity, bariatric surgery and lipid-lipoprotein metabolism/profile. 3-TYP clinical trial In this review, we described the metabolic impacts of different bariatric surgery procedures on the lipid-lipoprotein profile, and the mechanisms linking bariatric surgery and dyslipidemia remission based on recent epidemiological, clinical and preclinical studies. Fsitivity, liver fat content/function and lipid-lipoprotein metabolism.This study examined the influence of visual information of different complexities and predictability on the body sway of individuals with Parkinson's disease (PD) during upright stance. Twenty-one individuals at initial stages of PD (62.1 ± 7.2 years), under dopaminergic medication, and 21 controls (62.3 ± 7.1 years) stood inside a moving room, performing 10 trials of 60 s. In the first trial, the room remained motionless. Then, the room oscillated in an anterior-posterior direction. There were three blocks of three trials. In the first block, the room oscillated at 0.2 Hz (periodic simple condition); in the second block, periodic frequencies of 0.1, 0.3, and 0.5 Hz were combined (periodic complex condition); in the third block, non-periodic frequencies of 0.1, 0.3, and 0.5 Hz were combined (non-periodic complex condition). Participants were not informed about the room movement. The displacement of the room and trunk were registered using an OPTOTRAK system. Postural sway was examined using mean sway amplitude, and the relationship between visual information and body sway used coherence, gain, and phase. There was no group difference when the room remained motionless. Upon visual manipulation, the PD group displayed larger sway magnitude in the non-periodic complex condition. Individuals with PD also lagged behind the moving room (lower phase values) compared to controls, only in the periodic simple condition. In the remaining measures, there was no group difference. These results suggest that individuals with PD use complex and unpredictable visual information, similar to controls, during upright stance. However, PD might affect the predictable visual cues processing.Traumatic brain injury (TBI) is associated with increased blood content of fibrinogen (Fg), called hyperfibrinogenemia (HFg), which results in enhanced cerebrovascular permeability and leads to short-term memory (STM) reduction. Previously, we showed that extravasated Fg was deposited in the vasculo-astrocyte interface and was co-localized with cellular prion protein (PrPC) during mild-to-moderate TBI in mice. These effects were accompanied by neurodegeneration and STM reduction. However, there was no evidence presented that the described effects were the direct result of the HFg during TBI. We now present data indicating that inhibition of Fg synthesis can ameliorate TBI-induced cerebrovascular permeability and STM reduction. Cortical contusion injury (CCI) was induced in C57BL/6J mice. Then mice were treated with either Fg antisense oligonucleotide (Fg-ASO) or with control-ASO for two weeks. Cerebrovascular permeability to fluorescently labeled bovine serum albumin was assessed in cortical venules following evaluation of STM with memory assessement tests. Separately, brain samples were collected in order to define the expression of PrPC via Western blotting while deposition and co-localization of Fg and PrPC, as well as gene expression of inflammatory marker activating transcription factor 3 (ATF3), were characterized with real-time PCR. Results showed that inhibition of Fg synthesis with Fg-ASO reduced overexpression of AFT3, ameliorated enhanced cerebrovascular permeability, decreased expression of PrPC and Fg deposition, decreased formation of Fg-PrPC complexes in brain, and improved STM. These data provide direct evidence that a CCI-induced inflammation-mediated HFg could be a triggering mechanism involved in vascular cognitive impairment seen previously in our studies during mild-to-moderate TBI. This study aimed to examine the dynamic recovery of established multispecies biofilms of oral bacteria after an initial treatment by D-enantiomeric peptide DJK-5, L-enantiomeric peptide 1018, or chlorhexidine digluconate (CHX). Oral biofilms from 2 donors were grown on collagen-coated hydroxyapatite disks for 3 weeks and exposed to DJK-5, 1018, and 2% CHX for 3 minutes. Immediately after treatment and 1, 2, 3, 5, 7, 8, and 12 weeks after exposure, the biofilm volume and the volume ratio of dead and live bacteria in biofilms were assessed by confocal laser scanning microscopy using a live/dead viability stain. Results were examined by 1-way analysis of variance and post hoc multiple comparisons to determine significance at a P < .05 significance level. DJK-5 killed almost 80% of biofilms in 3 minutes and maintained this high level of dead bacteria for 1 week. The proportion of viable bacteria in DJK-5-treated biofilms returned to the pretreatment level after 12 weeks. The biovolume of DJK-5-treated biofilm remained significantly lower than that of biofilms after CHX and no treatment throughout the 12-week follow-up period (P < .