, malignancy risk, and centers' experience.A nanoformulation composed of curdlan, a linear polysaccharide of 1,3-β-linked d-glucose units, hydrogen bonded to poly(γ -glutamic acid) (PGA), was developed to stimulate macrophage. Curdlan/PGA nanoparticles (C-NP) are formulated by physically blending curdlan (0.2 mg mL-1 in 0.4 m NaOH) with PGA (0.8 mg mL-1 ). Forster resonance energy transfer (FRET) analysis demonstrates a heterospecies interpolymer complex formed between curdlan and PGA. The 1 H-NMR spectra display significant peak broadening as well as downfield chemical shifts of the hydroxyl proton resonances of curdlan, indicating potential intermolecular hydrogen bonding interactions. In addition, the cross peaks in 1 H-1 H 2D-NOESY suggest intermolecular associations between the OH-2/OH-4 hydroxyl groups of curdlan and the carboxylic-/amide-groups of PGA via hydrogen bonding. Intracellular uptake of C-NP occurs over time in human monocyte-derived macrophage (MDM). Furthermore, C-NP nanoparticles dose-dependently increase gene expression for TNF-α, IL-6, and IL-8 at 24 h in MDM. C-NP nanoparticles also stimulate the release of IL-lβ, MCP-1, TNF-α, IL-8, IL-12p70, IL-17, IL-18, and IL-23 from MDM. Overall, this is the first demonstration of a simplistic nanoformulation formed by hydrogen bonding between curdlan and PGA that modulates cytokine gene expression and release of cytokines from MDM.Human transcriptional enhanced associate domain (TEAD) family consists of four paralogous transcription factors that function to modulate gene expression by interacting with YAP-like coactivators and have been recognized as potential therapeutic targets of diverse diseases including lung cancer and gastric tumor. Here, we attempt to explore the systematic interaction profile between the 4 TEAD proteins and the peptides derived from the binding sites of 8 known YAP-like coactivators, in order to analyze the binding affinity and recognition specificity of these peptides toward the TEAD family, and to design hydrocarbon-stapled/cyclized peptides that can target the specific interaction profile for each coactivator. Structural, energetic, and dynamic investigations of TEAD-coactivator interactions reveal that the coactivators adopt three independent secondary structure regions (β-strand, α-helix, and Ω-loop) to surround on the surface of TEAD proteins, in which the α-helical and Ω-loop regions are primarily responsible for the interactions. Five α-helical peptides and four Ω-loop peptides are derived from the 8 YAP-like coactivators, and their systematic binding profile toward the 4 TEAD proteins is created, and hydrocarbon stapling and cyclization strategies are employed to constrain the free α-helical and Ω-loop peptides into their native conformations, respectively, thus effectively promoting peptide binding to TEADs. The all-hydrocarbon and disulfide bridges are designed to point out the TEAD-peptide complex interface, which would not disrupt the direct intermolecular interaction between the TEAD and peptide. Therefore, the stapling and cyclization only improve peptide binding affinity to these TEADs, but do not alter peptide recognition specificity over different TEADs.
  To compare surface topography of porcine and human root dentin and to develop a new in vitro model for class II furcation defects. The hypothesis for this study was that porcine mandible blocks can function as a model for class II furcation defects.
 
  Treatment of mandibular class II furcation defects is unpredictable. There is a need for in vitro models to investigate new treatment methods.
 
  A model to investigate the surface topography of porcine and human root dentin was developed and the two tissues compared by SEM imaging and profilometer. A novel method for studying class II furcation defects was then tested. Blocks of porcine mandibles with molar 3 were prepared. Buccal class II furcation defects were created. The furcation area was isolated and bioluminescent Staphylococcus epidermidis Xen43 was used to form a biofilm in the furcation area to test the functionality of the novel furcation model.
 
  Micromechanical damage caused by debridement on porcine and human root dentin showed similar pattern. No significant difference in the surface morphological parameters was observed between the corresponding porcine and human samples. The model allowed for assessment of the root surface inside the furcation area. While the number of viable bacteria in the furcation following debridement could be quantified, no significant difference between the treatment groups was detected, likely due to bacterial colonization within the periodontal ligament space.
 
  Porcine and human root dentin show similar surface topography following surface debridement. Porcine mandible blocks can function as a model for class II furcation defects. However, further development and refinement of the novel in vitro model is warranted.
 Porcine and human root dentin show similar surface topography following surface debridement.  https://www.selleckchem.com/  Porcine mandible blocks can function as a model for class II furcation defects. However, further development and refinement of the novel in vitro model is warranted.A rare case of omental torsion and infarct diagnosed on CT in a 63-year-old male with undifferentiated abdominal pain.
  This study aimed to evaluate the impact of coronavirus disease 2019 (Covid-19) outbreak on admissions for acute myocardial infarction (AMI) and related mortality, severity of presentation, major cardiac complications and outcome in a tertiary-care university hospital in Berlin, Germany.
 
  In a single-centre cross-sectional observational study, we included 355 patients with AMI containing ST-elevation or non-ST-elevation myocardial infarction (STEMI or NSTEMI), admitted for emergency cardiac catheterization between January and April 2020 and the equivalent time in 2019. During the early phase of the Covid-19 pandemic (e-COV) in Berlin (March and April 2020), admissions for AMI halved compared with those in the pre-Covid-19 time (January and February 2020; pre-COV) and with those in the corresponding months in 2019. However, mortality for AMI increased substantially from 5.2% pre-COV to 17.7% (P<0.05) during e-COV. Severity of presentation for AMI was more pronounced during e-COV [increased levels of cardiac enzymes, reduced left ventricular ejection fraction (LVEF), an increase in the need of inotropic support by 25% (P<0.