Hospital acquired venous thromboembolism (VTE) is a major source of morbidity and mortality, yet proven prevention measures are often underutilized. The lack of a validated VTE risk assessment model, difficulty integrating VTE risk assessment and prevention protocols into the routine process of care, and the lack of standardized metrics for VTE prophylaxis have all been barriers. Recently, a VTE risk assessment/prevention protocol has been validated, leading to portable strategies achieving breakthrough levels of adequate prophylaxis in a variety of inpatient settings. VTE prevention protocol design and implementation strategies have been collected in implementation guides available from the Society of Hospital Medicine and the Agency for Healthcare Research and Quality. These guides were the centerpieces of national collaborative efforts to improve VTE involving over 150 medical centers, honing the approach to accelerate improvement described in this article. Embedding a VTE prevention protocol into admission, transfer, and perioperative order sets is a key strategy. A VTE prevention protocol is defined as a VTE risk assessment with no more than three levels of risk, tightly linked to recommended prophylaxis for each level. A balance between the need to provide protocol guidance and the need for efficiency and ease-of-use by the clinician must be maintained. The power of this protocol driven approach is bolstered by a quality improvement framework, multidisciplinary teams, ongoing monitoring of the process, and real time identification and mitigation of non-adherents via a technique that measures progress and prompts concurrent intervention, an approach we call “measure-vention.”

Traditional hospital wards are not specifically designed as effective clinical microsystems. The feasibility and sustainability of doing so are unclear, as are the possible outcomes. To reorganize a traditional hospital ward with the traits of an effective clinical microsystem, we designed it to have 4 specific features: (1) unit‐based teams, (2) structured interdisciplinary bedside rounds, (3) unit‐level performance reporting, and (4) unit‐level nurse and physician coleadership. We called this type of unit an accountable care unit (ACU). In this narrative article, we describe our experience implementing each feature of the ACU. Our aim was to introduce a progressive approach to hospital care and training. Journal of Hospital Medicine 2015;10:36–40. © 2014 Society of Hospital Medicine

Tissue transglutaminase belongs to a family of calcium-dependent enzymes, the transglutaminases that catalyze the covalent cross-linking of specific proteins by the formation of epsilon (gamma-glutamyl)lysine isopeptide bonds. The goal of this study has been the isolation and characterization of the human tissue transglutaminase gene promoter. Genomic DNA clones, spanning the 5' region of the gene, were isolated and the structure of the 5'-end of the human tissue transglutaminase gene was determined. 1.74 kilobases of flanking DNA were sequenced and were found to contain a TATA box element (TATAA), a CAAT box element (GGACAAT), a series of potential transcription factor-binding sites (AP1, SP1, interleukin-6 response element), and a glucocorticoid response elements. Transient transfection experiments showed that this DNA fragment included a functional promoter, which is constitutively active in multiple cell types.

Tissue transglutaminase (transglutaminase type II) is an intracellular protein cross-linking enzyme that accumulates in connective tissue and in cells undergoing apoptosis. Retinoids regulate the transcription of the mouse tissue transglutaminase gene via activation of regulatory elements contained within 4 kilobases of the 5'-end of the gene. Co-transfection studies with retinoid receptor expression vectors in CV-1 cells demonstrated that the mouse tissue transglutaminase promoter is activated by ligand activation of either retinoic acid receptor-retinoid X receptor (RAR.RXR) heterodimers or RXR homodimers. Optimal induction is achieved with retinoid receptor panagonists; partial activation can also be achieved with either RAR-specific or RXR-specific retinoids. Retinoid-dependent activation of the tissue transglutaminase promoter depends on both a proximal regulatory region containing sequences highly conserved between the human and the mouse tissue transglutaminase promoters and a distal region that includes a 30-base pair retinoid response element (mTGRRE1). mTGRRE1 contains three hexanucleotide half-sites (two canonical and one non-canonical) in a DR7/DR5 motif that bind both RAR*RXR heterodimers and RXR homodimers. These studies suggest that retinoid-dependent expression of the mouse tissue transglutaminase gene is mediated by a versatile tripartite retinoid response element located 1.7 kilobases upstream of the transcription start site.

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