Procedure Cost Comparison of Outpatient and Inpatient Shoulder Arthroplasty and Lower-Extremity Arthroplasty Within a Managed-Care Organization.

Introduction The authors sought to evaluate cost differences between shoulder arthroplasties and lower-extremity joint replacements in the outpatient and inpatient setting within a large health-maintenance organization. Methods A cross-sectional study of 100 total hip arthroplasties (THA), 100 total knee arthroplasties (TKA), and 100 shoulder arthroplasties (50 anatomical total shoulder arthroplasties and 50 reverse shoulder arthroplasties [RTSA]) was performed at a single regional health care center within an integrated health care maintenance organization. A time-driven activity-based costing methodology was used to obtain total cost of each episode for outpatient (vs) inpatient surgery.

Author Correction: T-bet-dependent NKp46 innate lymphoid cells regulate the onset of T17-induced neuroinflammation.

In the version of this article initially published, in second paragraph of the second subsection of Results ('Peripheral licensing of CD4 T17 cells in Tbx21 hosts'), the figure citation ('Fig. 1c') in the sentence that begins "In addition to" was incorrect. The correct citation is 'Fig.

T-bet-dependent NKp46 innate lymphoid cells regulate the onset of T17-induced neuroinflammation.

The transcription factor T-bet has been associated with increased susceptibility to systemic and organ-specific autoimmunity, but the mechanism by which T-bet expression promotes neuroinflammation remains unknown. In this study, we demonstrate a cardinal role of T-bet-dependent NKp46 innate lymphoid cells (ILCs) in the initiation of CD4 T17-mediated neuroinflammation. Loss of T-bet specifically in NKp46 ILCs profoundly impaired the ability of myelin-reactive T17 cells to invade central nervous system (CNS) tissue and protected the mice from autoimmunity.

T-bet orchestrates CD8αα IEL differentiation.

Very little is known about the transcription factor network that regulates the development of intestinal intraepithelial lymphocytes (IELs). In this issue of Immunity, Klose et al. (2014b) and Reis et al.

Localized immunotherapy via liposome-anchored Anti-CD137 + IL-2 prevents lethal toxicity and elicits local and systemic antitumor immunity.

Immunostimulatory agonists such as anti-CD137 and interleukin (IL)-2 have elicited potent antitumor immune responses in preclinical studies, but their clinical use is limited by inflammatory toxicities that result upon systemic administration. We hypothesized that by rigorously restricting the biodistribution of immunotherapeutic agents to a locally accessible lesion and draining lymph node(s), effective local and systemic antitumor immunity could be achieved in the absence of systemic toxicity. We anchored anti-CD137 and an engineered IL-2Fc fusion protein to the surfaces of PEGylated liposomes, whose physical size permitted dissemination in the tumor parenchyma and tumor-draining lymph nodes but blocked entry into the systemic circulation following intratumoral injection.

Induction of potent anti-tumor responses while eliminating systemic side effects via liposome-anchored combinatorial immunotherapy.

Immunostimulatory therapies that activate immune response pathways are of great interest for overcoming the immunosuppression present in advanced tumors. Agonistic anti-CD40 antibodies and CpG oligonucleotides have previously demonstrated potent, synergistic anti-tumor effects, but their clinical use even as monotherapies is hampered by dose-limiting inflammatory toxicity provoked upon systemic exposure. We hypothesized that by anchoring immuno-agonist compounds to lipid nanoparticles we could retain the bioactivity of therapeutics in the local tumor tissue and tumor-draining lymph node, but limit systemic exposure to these potent molecules.

Cytosolic delivery of membrane-impermeable molecules in dendritic cells using pH-responsive core-shell nanoparticles.

Polycations that absorb protons in response to the acidification of endosomes can theoretically disrupt these vesicles via the "proton sponge" effect. To exploit this mechanism, we created nanoparticles with a segregated core-shell structure for efficient, noncytotoxic intracellular drug delivery. Cross-linked polymer nanoparticles were synthesized with a pH-responsive core and hydrophilic charged shell designed to disrupt endosomes and mediate drug/cell binding, respectively.