Splenectomy, still a commonly performed treatment for splenic injury in trauma patients, has been shown to have a high rate of complications. The purpose of this study was to identify predictors, including race and insurance status, associated with adverse outcomes post-splenectomy in trauma patients. We discuss possible explanations and methods for reducing these disparities.

Resection of many congenital lung lesions is commonly performed under single-lung ventilation, which helps collapse the lung being manipulated and enables a thoracoscopic approach in most cases. We set out to determine whether lung isolation achieved by either main stem intubation or usage of a bronchial blocker was associated with superior clinical outcomes. A retrospective review of all patients aged <2 years undergoing elective pulmonary lobectomy for congenital lung malformations at a tertiary-care pediatric hospital from 2011 through 2020 was performed. Demographic data, diagnosis type, type of lung isolation method employed, and perioperative outcomes were recorded. Continuous variables were analyzed with Student's -tests, whereas categorical variables were analyzed with Fisher's exact tests and chi-square tests. Thirty-two patients were analyzed-17 were managed with a bronchial blocker while 15 underwent main stem intubation. The most common diagnoses were congenital pulmonary airway malformations (53.1%) and intralobar bronchopulmonary sequestrations (34.4%). Patients managed with main stem intubation were slightly younger ( = .06) than those for which a bronchial blocker was used. Thirty-one (96.9%) resections were initiated thoracoscopically. Main stem intubation was associated with shorter operative times ( = .01), shorter anesthetic times ( = .02), and less blood loss ( = .04). No differences in length of stay ( = .64), conversation to thoracotomy ( = .35), intraoperative complications ( = .23), or postoperative complications ( = .49) were observed. Lung isolation through main stem intubation, when compared with bronchial blockers, is associated with shorter operative time, shorter anesthetic exposure, and diminished blood loss in pediatric patients undergoing lobectomy for congenital lung anomalies.

γδ T cells are important immunoregulatory cells in experimental autoimmune uveitis (EAU), and the activation status of γδ T cells determines their disease-enhancing or inhibitory effects. Because γδ T cells can be activated via various pathways, we questioned whether the nature of their activation might impact their function. In this study, we show that γδ T cells activated under different inflammatory conditions differ greatly in their functions. Whereas anti-CD3 treatment activated both IFN-γ and IL-17 γδ T cells, cytokines preferentially activated IL-17 γδ T cells. γδ T cells continued to express high levels of surface CD73 after exposure to inflammatory cytokines, but they downregulated surface CD73 after exposure to dendritic cells. Although both CD73 and CD73 cells have a disease-enhancing effect, the CD73 γδ T cells are less inhibitory. We also show that polarized activation not only applies to αβ T cells and myeloid cells, but also to γδ T cells. After activation under Th17-polarizing conditions, γδ T cells predominantly expressed IL-17 (gdT17), but after activation under Th1 polarizing conditions (gdT1) they mainly expressed IFN-γ. The pro-Th17 activity of γδ T cells was associated with gdT17, but not gdT1. Our results demonstrate that the functional activity of γδ T cells is strikingly modulated by their activation level, as well as the pathway through which they were activated.

Retinitis pigmentosa (RP) encompasses a group of inherited retinal dystrophies characterized by the primary degeneration of rod and cone photoreceptors. It is a leading cause of visual disability, with an incidence of ~1 in 7000 persons. Although most RP is nonsyndromic, 20%-30% of patients with RP also have an associated nonocular condition. The gene mutations responsible for RP occur overwhelmingly in rod photoreceptors. Visual loss frequently begins with night blindness in adolescence, followed by concentric visual field loss, reflecting the principal dysfunction of rod photoreceptors. Although the visual disability from rod dysfunction is significant, it is the subsequent loss of central vision later in life due to cone degeneration that is catastrophic. Until recently, the reason for cone dysfunction in RP was unknown. However, it is now recognized that cones degenerate, losing outer segment (OS) synthesis and inner segment (IS) disassembly because of glucose starvation following rod demise. Rod OS phagocytosis by the apical microvilli of retinal pigment epithelium is necessary to transport glucose from the choriocapillaris to the subretinal space. Although cones lose OS with the onset of rod degeneration in RP, regardless of the gene mutation in rods, cone nuclei remain viable for years (i.e. enter cone dormancy) so that therapies aimed at reversing glucose starvation can prevent and/or recover cone function and central vision.

Rhodopsin-mediated autosomal dominant retinitis pigmentosa (RP) is the most common cause of RP in North America. There is no proven cure for the disease, and multiple approaches are being studied. Gene therapy is an evolving field in medicine and ophthalmology. In this review, we will go over the basic concept of gene therapy and the different types of gene therapy that are currently being studied to treat this disease.