First, this study suggests that community engagement can play a role in redesigning a park and likely leads to increased awareness and use of neighborhood parks. Second, while park use increased, simply adding new features to a park may not immediately increase physical activity. Additional efforts need to be made to activate the park and increase physical activity. Third, practitioners should not discount the value of building park awareness that increases park use as it may be a first step to increasing physical activity.Thrombotic thrombocytopenic purpura (TTP) is a potentially fatal condition that can be challenging for clinicians to identify in the setting of autoimmune diseases such as systemic lupus erythematosus (SLE). This difficulty is compounded when a patient presents with all of the clinical signs of a TTP-like microangiopathy, however, with near normal ADAMTS13. This case report describes a 44-year-old female with a history of SLE who was hospitalized with acute on chronic anemia, thrombocytopenia, and altered mental status. The patient's ADAMTS13 was mildly low; hence, she was initially treated for SLE-associated immune thrombocytopenic purpura without any clinical response. The patient then underwent plasmapheresis (plasma exchange [PLEX]) for treatment of a suspected TTP-like microangiopathy. She responded to PLEX with improvement in her platelet count and mental status. This case illustrates the importance of considering TTP-like microangiopathic hemolytic anemia in the differential for patients with a history of SLE presenting with clinical signs of TTP even in the setting of near-normal ADAMTS13, thus warranting prompt treatment with PLEX.We report a rare case of a 32-year-old male who ingested 32.4 to 54 mg of colchicine and presented after 44 hours. He developed progressive multiple organ failure with shock, acute kidney failure, troponemia, pancytopenia, absolute neutropenia, disseminated intravascular coagulation, acute liver failure, rhabdomyolysis, and lactic acidosis. He also developed electrolyte abnormalities and refractory hypoglycemia. Initial treatment consisted of activated charcoal, fluids, and broad-spectrum antibiotics with supportive treatment of mechanical ventilation, hemodialysis, vasopressors, N-acetylcysteine, colony-stimulating factors, and blood products. Literature shows potential benefit of colchicine-specific Fab fragments for acute toxicity with limited studies and is not currently available in the United States. Further research for N-acetylcysteine protocol for acute liver failure in colchicine toxicity and potential use of colchicine-specific Fab fragments is needed. Our case demonstrates the importance of early use of activated charcoal for ingestion overdose with the incorporation of poison control into multidisciplinary team for coordinated patient care.
  Late gadolinium enhancement (LGE) cardiovascular magnetic resonance (CMR) imaging is the gold standard for noninvasive myocardial tissue characterization but requires intravenous contrast agent administration. It is highly desired to develop a contrast agent-free technology to replace LGE for faster and cheaper CMR scans.
 
  A CMR virtual native enhancement (VNE) imaging technology was developed using artificial intelligence. The deep learning model for generating VNE uses multiple streams of convolutional neural networks to exploit and enhance the existing signals in native T1 maps (pixel-wise maps of tissue T1 relaxation times) and cine imaging of cardiac structure and function, presenting them as LGE-equivalent images. The VNE generator was trained using generative adversarial networks. This technology was first developed on CMR datasets from the multicenter Hypertrophic Cardiomyopathy Registry, using hypertrophic cardiomyopathy as an exemplar. The datasets were randomized into 2 independent groups for deing and quantifying both hyperintensity myocardial lesions (
  =0.77-0.79; ICC=0.77-0.87; 
  <0.001) and intermediate-intensity lesions (
  =0.70-0.76; ICC=0.82-0.85; 
  <0.001). The native CMR images (cine plus T1 map) required for VNE can be acquired within 15 minutes and producing a VNE image takes less than 1 second.
 
  VNE is a new CMR technology that resembles conventional LGE but without the need for contrast administration. VNE achieved high agreement with LGE in the distribution and quantification of lesions, with significantly better image quality.
 VNE is a new CMR technology that resembles conventional LGE but without the need for contrast administration. VNE achieved high agreement with LGE in the distribution and quantification of lesions, with significantly better image quality.Aim To investigate the effect of rs3733846 in the flanking region of miR-143/145 on susceptibility to cervical squamous cell carcinoma (CSCC). Materials & methods We collected venous blood samples from 242 CSCC patients and 250 healthy controls. The rs3733846 polymorphism was genotyped by SnaPshot and Sanger sequencing.  https://www.selleckchem.com/peptide/box5.html  The expression of miR-143/145 in CSCC tissues was detected by quantitative real-time PCR. Results The rs3733846 AG genotype was associated with a decreased risk of CSCC in genetic model (AGvs.AA adjusted odds ratio [OR] 0.44; 95% CI 0.30-0.66; p less then 0.001). Patients with the rs3733846 AG/GG genotypes had a reduced risk of developing poorly differential status (OR 0.57; 95% CI 0.33-0.98; p less then 0.04) and lymph node metastasis (OR 0.49; 95% CI 0.26-0.92; p less then 0.03). Conclusion The rs3733846 in the flanking region of miR-143/145 was related to the susceptibility of CSCC.Background Current paradigms suggest that nitric oxide (NO) produced by endothelial cells (ECs) via endothelial nitric oxide synthase (eNOS) in the vessel wall is the primary regulator of blood flow and blood pressure. However, red blood cells (RBCs) also carry a catalytically active eNOS, but its role is controversial and remains undefined. This study aimed to elucidate the functional significance of red cell eNOS compared to EC eNOS for vascular hemodynamics and NO metabolism. Methods We generated tissue-specific "loss-" and "gain-of-function" models for eNOS by using cell-specific Cre-induced gene inactivation or reactivation. We created two founder lines carrying a floxed eNOS (eNOSflox/flox) for Cre-inducible knock out (KO), as well as gene construct with an inactivated floxed/inverted exon (eNOSinv/inv) for a Cre-inducible knock in (KI), which respectively allow targeted deletion or reactivation of eNOS in erythroid cells (RBC eNOS KO or RBC eNOS KI mice) or endothelial cells (EC eNOS KO or EC eNOS KI mice).