Clinical features, evaluation, and management of ophthalmic complications of facial paralysis: A review.

The purpose of this review was to study the evaluation, diagnosis, and management of ophthalmic complications associated with facial nerve palsy and to discuss the current and future interventions. The ophthalmic complications of facial paralysis include lagophthalmos, ectropion, exposure keratopathy, ocular synkinesis, and crocodile tears. Evaluation by an ophthalmologist skilled in recognizing and managing complications of facial paralysis shortly after its initial diagnosis can help identify and prevent long-term complications. Several types of grading scales are used to evaluate, measure the severity, and track surgical and patient-reported treatment outcomes. Lagophthalmos or ectropion are managed using temporary measures aimed at lubricating and covering the eye, including scleral lenses; however, these measures can be expensive and challenging to acquire and maintain. Temporary surgical interventions include lateral tarsorrhaphy, weighted eyelid implants, lateral canthoplasty, and other procedures that tighten or lift the eyelid or surrounding tissues. Management of flaccid facial paralysis due to iatrogenic injury or neoplasm requires neurorrhaphy or graft repair. The most common techniques for dynamic reconstruction in chronic facial paralysis are regional and free muscle flap transfer. Future directions for the management of ophthalmic complications aim to induce blinking and eye closure by developing systems that can detect blinking in the normal eye and transmit the signal to the paralyzed eye using mechanisms that would stimulate the muscles to induce eyelid closure. Blink detection technology has been developed, and a study demonstrated that blinking can be stimulated using electrodes on the zygomatic branch of the facial nerve. Further studies are needed to develop a system that will automate blinking and synchronize it with that of the normal eye.

A Virtual Curriculum to Increase Exposure to Oncologic Subspecialties for Undergraduate Medical Students.

Medical student exposure to oncology is imperative given the prevalence of cancer, growing need for survivorship care, and ever-evolving therapies. Our institution offers a Cancer Care Elective for undergraduate medical students focused on clinical shadowing, but the COVID-19 pandemic necessitated completely redesigning a virtual alternative. In this study, we utilize a post-elective survey to 1) assess whether the novel virtual elective effectively promoted student learning and 2) identify which components were most impactful. We created an entirely virtual, semester-long course with structured mentorship, subspecialty panels, physician-led didactics, and patient exposure. Students attended multidisciplinary tumor boards and presented on oncologic topics. A post-elective survey assessed the course's impact on students' knowledge and the perceived value of each elective component. Of the 29 enrolled students, 12 responded to our survey (41%). Most students reported that the elective highly enhanced their understanding of medical (67%), surgical (75%), and pediatric (66%) oncology. The highest rated didactic involved patients discussing their cancer journeys, with 80% of students reporting that this session enhanced their understanding of patient-physician collaboration. Students reported that physician mentorship helped them better understand oncology (90%) and promoted interest in pursuing an oncologic career (100%). This study demonstrates that our virtual Cancer Care Elective was effective at increasing student understanding of oncology in practice. The results also suggest that patient exposure and physician mentorship are particularly educational and encouraging.

Fecal microbiota of adolescent and young adult cancer survivors and metabolic syndrome: an exploratory study.

Metabolic syndrome and obesity occur commonly in long-term pediatric cancer survivors. The intestinal microbiome is associated with metabolic syndrome and obesity in the general population, and is perturbed during cancer therapy. We aimed to determine if long-term survivors of pediatric cancer would have reduced bacterial microbiome diversity, and if these findings would be associated with components of the metabolic syndrome, obesity, and chronic inflammation. We performed a cross-sectional exploratory study examining the intestinal microbiome via 16S amplicon sequencing, treatment history, clinical measurements (blood pressure, body mass index) and biomarkers (hemoglobin A1c, lipoproteins, adiponectin: leptin ratio, C-reactive protein, TNFα, Interleukin-6, and Interleukin-10) between 35 long-term survivors and 32 age, sex, and race matched controls. All subjects were aged 10-40 years, and survivors were at least five years from therapy completion. Survivors had lower alpha diversity compared to controls (Shannon index p = .001, Simpson index p = .032) and differently abundant bacterial taxa. Further, among survivors, those who received radiation (18/35) to the central nervous system or abdomen/pelvis had decreased alpha diversity compared to those who did not receive radiation (Shannon and Simpson p < .05 for both). Although, no specific component of metabolic syndrome or cytokine was associated with measures of alpha diversity, survivors with low adiponectin-lectin ratio, elevated body mass index, and elevated C-reactive protein had differently abundant taxa compared to those with normal measures. The microbiome of cancer survivors remains less diverse than controls even many years after diagnosis, and exposure to radiation may lead to further loss of diversity in survivors.Supplemental data for this article is available online at https://doi.org/10.1080/08880018.2022.2049937.

MYC drives overexpression of telomerase RNA (hTR/TERC) in prostate cancer.

Telomerase consists of at least two essential elements, an RNA component hTR or TERC that contains the template for telomere DNA addition and a catalytic reverse transcriptase (TERT). While expression of TERT has been considered the key rate-limiting component for telomerase activity, increasing evidence suggests an important role for the regulation of TERC in telomere maintenance and perhaps other functions in human cancer. By using three orthogonal methods including RNAseq, RT-qPCR, and an analytically validated chromogenic RNA in situ hybridization assay, we report consistent overexpression of TERC in prostate cancer. This overexpression occurs at the precursor stage (e.g. high-grade prostatic intraepithelial neoplasia or PIN) and persists throughout all stages of disease progression. Levels of TERC correlate with levels of MYC (a known driver of prostate cancer) in clinical samples and we also show the following: forced reductions of MYC result in decreased TERC levels in eight cancer cell lines (prostate, lung, breast, and colorectal); forced overexpression of MYC in PCa cell lines, and in the mouse prostate, results in increased TERC levels; human TERC promoter activity is decreased after MYC silencing; and MYC occupies the TERC locus as assessed by chromatin immunoprecipitation (ChIP). Finally, we show that knockdown of TERC by siRNA results in reduced proliferation of prostate cancer cell lines. These studies indicate that TERC is consistently overexpressed in all stages of prostatic adenocarcinoma and that its expression is regulated by MYC. These findings nominate TERC as a novel prostate cancer biomarker and therapeutic target. Copyright © 2017 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.