Evaluation of Prescribing and Administering As-Needed Pain Medications Based on Pain Severity Scores.

Pain is a common symptom reported by patients admitted to hospitals in both medical and surgical units. Due to the subjective and multidimensional nature of pain, it should be assessed regularly to ensure patient pain control. Suboptimal prescribing of opioids and other pain medications contribute to the inadequate treatment of pain.

Effectiveness of dietary inorganic nitrate for lowering blood pressure in hypertensive adults: a systematic review.

Objective: The objective of this review was to evaluate the effectiveness of inorganic nitrate on blood pressure in hypertensive adults.

Introduction: Hypertension is associated with increased risk of morbidity and mortality in adults. Inorganic nitrate could be beneficial for lowering blood pressure and reducing cardiovascular disease risks.

Effectiveness of dietary inorganic nitrate in lowering blood pressure in hypertensive adults: a systematic review protocol.

The question of this review is: what is the effect of dietary inorganic nitrate on blood pressure in adults with blood pressure >120/80mmHg?

Injection of recombinant human type VII collagen corrects the disease phenotype in a murine model of dystrophic epidermolysis bullosa.

Patients with recessive dystrophic epidermolysis bullosa (RDEB) have incurable skin fragility, blistering, and scarring due to mutations in the gene that encodes for type VII collagen (C7) that mediates dermal-epidermal adherence in human skin. We showed previously that intradermal injection of recombinant C7 into transplanted human DEB skin equivalents stably restored C7 expression at the basement membrane zone (BMZ) and reversed the RDEB disease features. In this study, we evaluated the feasibility of protein therapy in a C7 null mouse (Col7a1(-/-)) which recapitulates the features of human RDEB.

Autoimmunity to type VII collagen: epidermolysis bullosa acquisita.

Epidermolysis bullosa acquisita (EBA) is an acquired, mechanobullous disease characterized by autoimmunity to type VII collagen. Type VII collagen makes anchoring fibrils, structures that connect the epidermis and its underlying basement membrane zone to the papillary dermis. EBA patients exhibit skin fragility, blisters, scars and milia formation reminiscent of genetic dystrophic epidermolysis bullosa (DEB).

Autoimmunity to type VII collagen: epidermolysis bullosa acquisita.

Epidermolysis bullosa acquisita (EBA) is an acquired, autoimmune, mechanobullous disease with clinical features reminiscent of genetic dystrophic epidermolysis bullosa (DEB). EBA patients have skin fragility, blisters, scars, and milia formation. DEB is due to a genetic defect in the gene-encoding type VII collagen, which makes anchoring fibrils, structures that attach the epidermis and its underlying basement membrane zone onto the papillary dermis.

The cartilage matrix protein subdomain of type VII collagen is pathogenic for epidermolysis bullosa acquisita.

Epidermolysis bullosa acquisita (EBA) is an acquired bullous disease of the skin characterized by IgG autoantibodies against type VII (anchoring fibril) collagen. We previously defined four immunodominant antigenic epitopes within the noncollagenous 1 (NC1) domain of type VII collagen. In this study, we produced an additional recombinant fusion protein from the NC1 domain corresponding to the N-terminal 227 amino acids (residues 1 to 227), which contains homology with cartilage matrix protein (CMP).

Intravenously injected human fibroblasts home to skin wounds, deliver type VII collagen, and promote wound healing.

Patients with dystrophic epidermolysis bullosa (DEB) have incurable skin fragility, blistering, and multiple skin wounds because of mutations in the gene that encodes for type VII collagen (C7), which holds together the epidermal and dermal layers of human skin. The intradermal injection of gene-corrected DEB fibroblasts, recombinant C7 protein, or lentiviral vectors expressing C7 is a potential therapy for DEB. Nevertheless, severe DEB causes widespread wounds and treatment would require multiple injections.

Induction of epidermolysis bullosa acquisita in mice by passive transfer of autoantibodies from patients.

Epidermolysis bullosa acquisita (EBA) is an autoimmune sub-epidermal blistering disease characterized by autoantibodies to type VII (anchoring fibril) collagen. To date, however, direct evidence for a pathogenic role of human EBA autoantibodies has not been demonstrated. In this study, we affinity-purified anti-type VII collagen antibodies from EBA patients' sera and then injected them into adult hairless immunocompetent mice.