Limited Audiological Assessment Results in Children With Otitis Media With Effusion.

Objectives: Clinical practice guidelines predicate the need for evaluation of hearing in children with otitis media with effusion (OME). The objective of this work was to characterize the completeness of hearing assessment results in children with OME.

Design: Forty participants with OME completed two full audiological assessments, one in a clinical setting and a second in a research setting.

Audiologic Profiles of Children With Otitis Media With Effusion.

Objectives: To describe the impact of effusion volume, viscosity, and purulence on the audiologic profiles of children with otitis media with effusion.

Design: Fifty-one ears from children between the ages of 8 months and 11 years who had a diagnosis of otitis media with effusion and were scheduled for tympanostomy tube placement were recruited from medical clinics. The control group consisted of 17 ears from children between the ages of 10 months and 11 years without a recent history of otitis media and were recruited from a database of research volunteers.

Improving the Differential Diagnosis of Otitis Media With Effusion Using Wideband Acoustic Immittance.

Objectives: The objective of this work is to determine whether there is a systematic effect of middle ear effusion volume on wideband acoustic immittance in children with surgically confirmed otitis media with effusion.

Design: Wideband acoustic immittance was measured in 49 ears from children (9 months to 11 years) who had a diagnosis of otitis media with effusion and compared to 14 ears from children (10 months to 10 years) without a recent history of otitis media. For children with otitis media with effusion, wideband acoustic immittance testing took place in the child's preoperative waiting room before surgical placement of tympanostomy tubes.

Invariant asymmetry renews the lymphatic vasculature during homeostasis.

Background: The lymphatic vasculature regulates tissue physiology and immunity throughout life. The self renewal mechanism that maintains the lymphatic vasculature during conditions of homeostasis is unknown. The purpose of this study was to investigate the cellular mechanism of lymphatic endothelial cell (LEC) self renewal and lymphatic vessel maintenance.

Lymphatic endothelial lineage assemblage during corneal lymphangiogenesis.

Postnatal inflammatory lymphangiogenesis presumably requires precise regulatory processes to properly assemble proliferating lymphatic endothelial cells (LECs). The specific mechanisms that regulate the assembly of LECs during new lymphatic vessel synthesis are unclear. Dynamic endothelial shuffling and rearrangement has been proposed as a mechanism of blood vessel growth.

Nerve growth factor regulates neurolymphatic remodeling during corneal inflammation and resolution.

The cellular and physiologic mechanisms that regulate the resolution of inflammation remain poorly defined despite their widespread importance in improving inflammatory disease outcomes. We studied the resolution of two cardinal signs of inflammation-pain and swelling-by investigating molecular mechanisms that regulate neural and lymphatic vessel remodeling during the resolution of corneal inflammation. A mouse model of corneal inflammation and wound recovery was developed to study this process in vivo.

Lymphatic vessel memory stimulated by recurrent inflammation.

Inflammation stimulates new lymphatic vessel growth (inflammatory lymphangiogenesis). One key question is how recurrent inflammation, a common clinical condition, regulates lymphatic vessel remodeling. We show here that recurrent inflammation accelerated the development a functional lymphatic vessel network.

Glucocorticoids suppress corneal lymphangiogenesis.

Purpose: To determine whether glucocorticoids suppress corneal lymphatic vessel growth (lymphangiogenesis) or induce lymphatic vessel regression.

Methods: We measured human lymphatic endothelial cell proliferation and collagen-induced tubulogenesis in culture conditions with and without dexamethasone, a potent glucocorticoid. We developed a modification of the mouse corneal suture model that allowed us to visualize lymphatic vessel growth (with suture) or regression (suture removed) using immunofluorescence and microscopic techniques.

Regressed lymphatic vessels develop during corneal repair.

The fate of newly synthesized lymphatic vessels induced by inflammation is poorly understood. To address this question, we designed experiments to determine the morphologic, phenotypic, and functional differences in regressing lymphatic vessels in the context of corneal recovery after an inflammatory response. A suture removal modification was used to induce corneal recovery after suture induced inflammation.

β1 integrin regulates MMP-10 dependant tubulogenesis in human lymphatic endothelial cells.

Lymphatic vessel growth requires extensive remodeling of the extracellular matrix, a process hypothesized to be related to the expression and function of the matrix metalloproteinases. We used a protein based screening strategy to demonstrate increased matrix matalloproteinase-10 expression in human lymphatic endothelial cells undergoing collagen I induced tubulogenesis. Knock-down experiments showed that matrix metalloproteinase-10 regulated lymphatic endothelial cell tubulogenesis.

Lymphatic vessel hypertrophy in inflamed human tonsils.

The structural and molecular properties of the human tonsil lymphatic microvascular system are important to understand as these features likely contribute to fluid balance, immunity, and tumor metastasis. The tonsil is a unique lymphoid organ in that it is in intimate contact with the contents of the upper aerodigestive tract and that there are no identifiable afferent lymphatics. Conventional immunofluorescence microscopy demonstrated a remarkable degree of lymphatic vessel architecture within the tonsil; LYVE-1-positive lymphatic vessels were detected around each germinal center and in the marginal regions between the follicles.

Lymphatic malformations: review of current treatment.

Objective: Summarize current knowledge of lymphatic malformation medical, sclerotherapy, and surgical treatment; and highlight areas of treatment controversy and treatment difficulty that need improvement.

Methods: Panel presentation of various aspects of lymphatic malformation treatment.

Results: The mainstay of lymphatic malformation treatment has been surgical resection, which has been refined through lesion staging and radiographic characterization.

Lymphatic malformations: current cellular and clinical investigations.

Objective: Summarize current knowledge of lymphatic malformation development, biology, and clinical outcome measures.

Methods: Panel presentation of lymphatic malformation biology and measurement of head and neck malformation treatment outcomes.

Results: Characterization of lymphatic malformation endothelial and stromal cells may lead to biologically based treatment.

Integrin alpha1beta1 regulates matrix metalloproteinases via P38 mitogen-activated protein kinase in mesangial cells: implications for Alport syndrome.

Previous work has shown that integrin alpha1-null Alport mice exhibit attenuated glomerular disease with decreased matrix accumulation and live much longer than strain-matched Alport mice. However, the mechanism underlying this observation is unknown. Here we show that glomerular gelatinase expression, specifically matrix metalloproteinase-2 (MMP-2), MMP-9, and MMP-14, was significantly elevated in both integrin alpha1-null mice and integrin alpha1-null Alport mice relative to wild-type mice; however, only MMP-9 was elevated in glomeruli of Alport mice that express integrin alpha1.

Clinical outcomes in lymphocytopenic lymphatic malformation patients.

Background: To determine if lymphocytopenia in patients with lymphatic malformation (LM) is associated with rates of infection and poor clinical outcomes.

Materials And Methods: This is a retrospective case series at a tertiary pediatric hospital, of 21 consecutive patients (11 male and 10 female) undergoing LM treatment. Clinical data (i.

Lymphocytopenia in children with lymphatic malformation.

Objective: To determine whether an immunologic abnormality exists in patients with lymphatic malformation (LM).

Design: Retrospective case series.

Setting: Tertiary care pediatric hospital.

Proliferation and differentiation of CD8+ T cells in the absence of IL-2/15 receptor beta-chain expression or STAT5 activation.

Major gains in the efficacy of T cell-based therapies for cancer and infectious diseases could be realized through improved understanding of the signals that control expansion and differentiation of CD8(+) cytolytic T cells. IL-2, IL-15, and the downstream transcription factor STAT5 have all been implicated as important regulators of these processes, yet there are conflicting data regarding their contribution to in vivo T cell responses. We used a murine adoptive T cell transfer model to examine the contribution of IL-2 and IL-15 signaling to the proliferation and differentiation of naive, CD8(+) T cells bearing an OVA-specific TCR transgene (OT-I).

MUC1-specific anti-tumor responses: molecular requirements for CD4-mediated responses.

MUC1 was first defined as a tumor antigen in the late 1980s, yet little is known about the types of immune responses that mediate rejection of MUC1(+) tumors in vivo. MUC1-specific antibodies, T(h) cells and cytotoxic T cells can be detected in patients with different adenocarcinomas, yet these tumors usually progress. Thus, there is a need to better understand the in vivo mechanisms of antigen-specific tumor rejection.

Molecular requirements for CD8-mediated rejection of a MUC1-expressing pancreatic carcinoma: implications for tumor vaccines.

Previous studies have indicated that different effector cells are required to eliminate MUC1-expressing tumors derived from different organ sites and that different vaccine strategies may be necessary to generate these two different MUC1-specific immune responses. In this study, we characterized molecular components that are required to produce immune responses that eliminate Panc02.MUC1 tumors in vivo by utilizing mice genetically deficient in molecules related to immunity.