A 52-year-oldintellectually disabled man who had previously undergone a left canal wall down mastoidectomy with cartilage graft tympanoplasty for cholesteatoma 20 years ago presented with new-onset discharge in the contralateral ear. He did not have any symptoms, particularly recurrent discharge, in the post-operative ear, despite infrequent and irregular clinic follow-up for periodic cleaning of the cavity. Clinical examination of the post-operative ear revealed the presence of retained cerumen which was easily removed. The mastoid cavity was noted to have a healthy skin lining, an intact neotympanum, and a smooth bowl-like appearance with no areas that could not be adequately visualized through the surgically widened external auditory meatus. He underwent computerized tomographic imaging of the temporal bone to evaluate the nature and cause of the new-onset discharge in the contralateral ear. This imaging study provided the opportunity to present and describe key post-operative radiologic features of a symptom-free canal-wall down mastoidectomy with tympanoplasty.

A canal-wall down mastoidectomy is a more extensive type of mastoidectomy which, in addition to the resection of the mastoid cortex, all mastoid air cells and Körner septum, is characterized by the resection of the posterior wall of the external auditory canal and scutum. Among the most common causes of failure following this type of surgery are incomplete removal of tegmental air cells and incomplete lowering of the facial ridge.1These two factors can and should be purposefully assessed in a post-operative imaging study.

Adequacy of bone removal in the epitympanum to address the issue of tegmental air cell disease is evaluated on axial CT images at the level of the malleus head-incus body complex and the proximal portion of the tympanic segment of the facial nerve. (Figure 1) All of the bone lateral to the ossicles, especially that overlying the malleus head and anterior epitympanic recess, should have been surgically removed.

On coronal CT images, this same adequacy is demonstrated by the surgical removal of all bone lateral to the epitympanum, from the scutum to the outer cortex, such that there is a clear line of sight from the external auditory meatus to the epitympanum. This helps ensure that there are no pockets of soft tissue medial to any bony ridges; soft tissue that may represent residual or recurrent disease. (Figure 2)

Background: Type 1 diabetes (T1D) results in autoreactive T cells chronically destroying pancreatic islets. This often results in irreplaceable loss of insulin-producing beta cells. To reverse course, a combinatorial strategy of employing glucose-responsive insulin restoration coupled with inhibiting autoreactive immune responses is required. Methods: Non-obese diabetic mice received a single intraperitoneal implantation of a novel biomaterial co-seeded with insulin-producing islets and T regulatory cells (Tregs). Controls included biomaterial seeded solely with islets, or biomaterial only groups. Mice were interrogated for changes in inflammation and diabetes progression via blood glucose monitoring, multiplex serum cytokine profiling, flow cytometry and immunohistochemistry assessments. Results: Islet and Tregs co-seeded biomaterial recipients had increased longevity, insulin secretion, and normoglycemia through 180 days post-implantation compared to controls. Serum profile revealed reduced TNFα, IFNγ, IL-1β and increased IL-10, insulin, C-Peptide, PP and PPY in recipients receiving co-seeded biomaterial. Evaluation of the resected co-seeded biomaterial revealed reduced infiltrating autoreactive CD8 + and CD4 + T cells concomitant with sustained presence of Foxp3 + Tregs; further analysis revealed that the few infiltrated resident effector CD4+ or CD8+ T cells were anergic, as measured by low levels of IFNγ and Granzyme-B upon stimulation when compared to controls. Interestingly, studies also revealed increased Tregs in the pancreas. However, there was no restoration of the pancreas beta cell compartment, suggesting normoglycemia and production of insulin levels were largely supported by the implanted co-seeded biomaterial. Conclusion These studies show the efficacy of a combinatorial approach seeding Tregs with pancreatic islets in a novel self-assembling organoid for reversing T1D.

Background: Type 1 diabetes (T1D) results in autoreactive T cells chronically destroying pancreatic islets. This often results in irreplaceable loss of insulin-producing beta cells. To reverse course, a combinatorial strategy of employing glucose-responsive insulin restoration coupled with inhibiting autoreactive immune responses is required. Methods: Non-obese diabetic mice received a single intraperitoneal implantation of a novel biomaterial co-seeded with insulin-producing islets and T regulatory cells (Tregs). Controls included biomaterial seeded solely with islets, or biomaterial only groups. Mice were interrogated for changes in inflammation and diabetes progression via blood glucose monitoring, multiplex serum cytokine profiling, flow cytometry and immunohistochemistry assessments. Results: Islet and Tregs co-seeded biomaterial recipients had increased longevity, insulin secretion, and normoglycemia through 180 days post-implantation compared to controls. Serum profile revealed reduced TNFα, IFNγ, IL-1β and increased IL-10, insulin, C-Peptide, PP and PPY in recipients receiving co-seeded biomaterial. Evaluation of the resected co-seeded biomaterial revealed reduced infiltrating autoreactive CD8 + and CD4 + T cells concomitant with sustained presence of Foxp3 + Tregs; further analysis revealed that the few infiltrated resident effector CD4+ or CD8+ T cells were anergic, as measured by low levels of IFNγ and Granzyme-B upon stimulation when compared to controls. Interestingly, studies also revealed increased Tregs in the pancreas. However, there was no restoration of the pancreas beta cell compartment, suggesting normoglycemia and production of insulin levels were largely supported by the implanted co-seeded biomaterial. Conclusion These studies show the efficacy of a combinatorial approach seeding Tregs with pancreatic islets in a novel self-assembling organoid for reversing T1D.

Background: Type 1 diabetes (T1D) results in autoreactive T cells chronically destroying pancreatic islets. This often results in irreplaceable loss of insulin-producing beta cells. To reverse course, a combinatorial strategy of employing glucose-responsive insulin restoration coupled with inhibiting autoreactive immune responses is required. Methods: Non-obese diabetic mice received a single intraperitoneal implantation of a novel biomaterial co-seeded with insulin-producing islets and T regulatory cells (Tregs). Controls included biomaterial seeded solely with islets, or biomaterial only groups. Mice were interrogated for changes in inflammation and diabetes progression via blood glucose monitoring, multiplex serum cytokine profiling, flow cytometry and immunohistochemistry assessments. Results: Islet and Tregs co-seeded biomaterial recipients had increased longevity, insulin secretion, and normoglycemia through 180 days post-implantation compared to controls. Serum profile revealed reduced TNFα, IFNγ, IL-1β and increased IL-10, insulin, C-Peptide, PP and PPY in recipients receiving co-seeded biomaterial. Evaluation of the resected co-seeded biomaterial revealed reduced infiltrating autoreactive CD8 + and CD4 + T cells concomitant with sustained presence of Foxp3 + Tregs; further analysis revealed that the few infiltrated resident effector CD4+ or CD8+ T cells were anergic, as measured by low levels of IFNγ and Granzyme-B upon stimulation when compared to controls. Interestingly, studies also revealed increased Tregs in the pancreas. However, there was no restoration of the pancreas beta cell compartment, suggesting normoglycemia and production of insulin levels were largely supported by the implanted co-seeded biomaterial. Conclusion These studies show the efficacy of a combinatorial approach seeding Tregs with pancreatic islets in a novel self-assembling organoid for reversing T1D.

Background: Type 1 diabetes (T1D) results in autoreactive T cells chronically destroying pancreatic islets. This often results in irreplaceable loss of insulin-producing beta cells. To reverse course, a combinatorial strategy of employing glucose-responsive insulin restoration coupled with inhibiting autoreactive immune responses is required. Methods: Non-obese diabetic mice received a single intraperitoneal implantation of a novel biomaterial co-seeded with insulin-producing islets and T regulatory cells (Tregs). Controls included biomaterial seeded solely with islets, or biomaterial only groups. Mice were interrogated for changes in inflammation and diabetes progression via blood glucose monitoring, multiplex serum cytokine profiling, flow cytometry and immunohistochemistry assessments. Results: Islet and Tregs co-seeded biomaterial recipients had increased longevity, insulin secretion, and normoglycemia through 180 days post-implantation compared to controls. Serum profile revealed reduced TNFα, IFNγ, IL-1β and increased IL-10, insulin, C-Peptide, PP and PPY in recipients receiving co-seeded biomaterial. Evaluation of the resected co-seeded biomaterial revealed reduced infiltrating autoreactive CD8 + and CD4 + T cells concomitant with sustained presence of Foxp3 + Tregs; further analysis revealed that the few infiltrated resident effector CD4+ or CD8+ T cells were anergic, as measured by low levels of IFNγ and Granzyme-B upon stimulation when compared to controls. Interestingly, studies also revealed increased Tregs in the pancreas. However, there was no restoration of the pancreas beta cell compartment, suggesting normoglycemia and production of insulin levels were largely supported by the implanted co-seeded biomaterial. Conclusion These studies show the efficacy of a combinatorial approach seeding Tregs with pancreatic islets in a novel self-assembling organoid for reversing T1D.

Background: Type 1 diabetes (T1D) results in autoreactive T cells chronically destroying pancreatic islets. This often results in irreplaceable loss of insulin-producing beta cells. To reverse course, a combinatorial strategy of employing glucose-responsive insulin restoration coupled with inhibiting autoreactive immune responses is required. Methods: Non-obese diabetic mice received a single intraperitoneal implantation of a novel biomaterial co-seeded with insulin-producing islets and T regulatory cells (Tregs). Controls included biomaterial seeded solely with islets, or biomaterial only groups. Mice were interrogated for changes in inflammation and diabetes progression via blood glucose monitoring, multiplex serum cytokine profiling, flow cytometry and immunohistochemistry assessments. Results: Islet and Tregs co-seeded biomaterial recipients had increased longevity, insulin secretion, and normoglycemia through 180 days post-implantation compared to controls. Serum profile revealed reduced TNFα, IFNγ, IL-1β and increased IL-10, insulin, C-Peptide, PP and PPY in recipients receiving co-seeded biomaterial. Evaluation of the resected co-seeded biomaterial revealed reduced infiltrating autoreactive CD8 + and CD4 + T cells concomitant with sustained presence of Foxp3 + Tregs; further analysis revealed that the few infiltrated resident effector CD4+ or CD8+ T cells were anergic, as measured by low levels of IFNγ and Granzyme-B upon stimulation when compared to controls. Interestingly, studies also revealed increased Tregs in the pancreas. However, there was no restoration of the pancreas beta cell compartment, suggesting normoglycemia and production of insulin levels were largely supported by the implanted co-seeded biomaterial. Conclusion These studies show the efficacy of a combinatorial approach seeding Tregs with pancreatic islets in a novel self-assembling organoid for reversing T1D.

A 2-month-old baby girl presented with a failed neonatal otoacoustic emission (OAE) hearing screening in the left ear. Combined Auditory Brainstem Response/Auditory Steady-State Response (ABR/ASSR) testing confirmed the presence of a unilateral left moderate to severe hearing loss. No Joint Committee on Infant Hearing (JCIH) risk factors for early childhood hearing loss1 were identified. She subsequently underwent computed tomography (CT) of the temporal bones to determine the presence of any inner ear malformation. No abnormalities of the internal auditory canal, cochlea, semicircular canals and ossicles were noted by the radiologist, and the study was officially reported as a “normal temporal bone CT scan.” Independent review of the CT imaging revealed the presence of a visually apparent disparity in the width of the cochlear nerve canals. (Figure 1) Measurement of the cochlear nerve canal width in the axial plane parallel to the infraorbitomeatal line2 using the length measurement tool in the DICOM imaging software (RadiAnt DICOM Viewer, Version 2024.1, Medixant) indicated a cochlear nerve canal width of 2.18 mm on the right and 1.02 mm on the left. (Figure 2) Applying the suggested cutoff point of 1.2 mm as described by Lin et al.,2 we identified the presence of left cochlear nerve canal stenosis as the etiology of the congenital unilateral hearing loss. The cochlear nerve canal, which has also been referred to as the bony canal for the cochlear nerve (BCNC), cochlear aperture, and cochlear fosette, is the bony transition point between the internal auditory canal and the cochlear modiolus. A relationship between a hypoplastic cochlear nerve canal and congenital sensorineural hearing loss was first suggested by Fatterpekar et al. in 2000.3 Subsequent studies confirmed the association between cochlear nerve canal stenosis and sensorineural hearing loss that ranges from near-normal to profound, with a statistically significant relationship between the degree of hearing loss and the degree of stenosis.4 Various cutoff points to define stenosis of the cochlear nerve canal have been identified in the medical literature. These cutoff points range from 1.2 mm to 1.7 mm when the canal width is measured in the axial plane.2 This particular case demonstrated clear-cut evidence of cochlear nerve canal stenosis, as it satisfied the smallest cutoff criteria (< 1.2 mm) seen in the medical literature. The identification of cochlear nerve canal stenosis as the cause of congenital sensorineural hearing loss is important not only from a diagnostic point, but also from a prognostic perspective. Cochlear nerve deficiency has been noted to be highly prevalent among pediatric patients with cochlear nerve canal stenosis,5 and this has significant negative implications in relation to rehabilitation with external hearing devices and cochlear implants.