Follow-up Adherence and Barriers to Care for Pediatric Glaucomas at a Tertiary Care Center.

PURPOSE: To determine the percent adherence to follow-up for patients with pediatric glaucomas seen at a tertiary care center and to elucidate risk factors. DESIGN: Retrospective cohort study. METHODS: Patients with pediatric glaucomas seen at the University of Minnesota over 8.5 years were classified as adherent, nonadherent, or lost to tertiary follow-up if they followed up within 0-30 days, between 31 and 180 days, or later than 180 days of the recommended appointment time or never, respectively. RESULTS: Of 176 patients analyzed, 95 (54%) were adherent (51% male; mean [standard deviation (SD)] age: 56.1 [59.8] months), 5 (3%) were nonadherent (20% male; mean [SD] age: 25.0 [35.8] months), and 76 (43%) were lost to tertiary follow-up (55% male; mean [SD] age: 58.9 [53.1] months). Multiple logistic regression analysis of variables that were significant in isolation revealed that only race (white: odds ratio, 3.58; 95% confidence interval, 1.42-9.05; P = .007) and distance from the eye clinic (per 50 miles: odds ratio, 0.79; 95% confidence interval, 0.67-0.92; P = .003) significantly impacted adherence. CONCLUSIONS: This is the first study of adherence to follow-up recommendations for patients with pediatric glaucomas. Percent adherence to follow-up appointments was alarmingly low, and decreased adherence was observed with non-white race and increased distance to the eye clinic. Physicians should consider these risk factors when risk-stratifying patients with pediatric glaucomas for nonadherence to follow-up. Additional studies to improve adherence through interventions that reduce biases and barriers to follow-up are needed.

Effect of the Affordable Care Act on a Safety-Net Burn Center.

We hypothesized that the Patient Protection and Affordable Care Act (ACA) would have beneficial financial effects on our burn center at a safety-net hospital. We performed a retrospective chart review of all burn patients admitted to our center from 2008-2016. These were further divided into three time periods: 2008-2010 (pre-ACA), 2011-2013 (transitional), and 2014-2016 (post-ACA). Cost and reimbursement dollars were adjusted to health personal consumption expenditures price index. Total charges increased from the pre-ACA group ($69,400) to the transitional group ($85,600) and increased again in the post-ACA group ($100,100) (p<.001). When looking at reimbursements relative to charges, actual reimbursement by percentage dropped over each time period. Despite an increase in insured patients, our burn center actually saw a decrease in reimbursements relative to billing.

Human papillomavirus in oropharyngeal squamous cell carcinoma: assessing virus presence in normal tissue and activity in cervical metastasis.

OBJECTIVES/HYPOTHESIS: Human papillomavirus (HPV) has been established as an etiologic and prognostic factor in oropharyngeal squamous cell carcinoma (OPSCC). HPV oncogenesis involves expression of E6/E7 oncoproteins, with downstream p53 degradation and pRb inhibition. Although much research has focused on HPV's oncogenic behavior in primary OPSCC, minimal information exists about HPV in adjacent normal and metastatic tissue. STUDY DESIGN: Retrospective cohort study METHODS: Patient-matched tumor, normal, and metastatic tissue was gathered from 42 OPSCC patients and tested with real-time quantitative polymerase chain reaction (RT-qPCR), in situ hybridization (ISH), and immunohistochemistry (IHC). RT-qPCR was performed using total RNA from fresh-frozen tissues and primers for HPV16 E6, E7, and p16 transcripts. HPV ISH was performed to detect the presence of HPV DNA and IHC to detect p16 protein. RESULTS: Primary tumor, adjacent normal tissue, and tumor metastasis from 17 OPSCC patients were analyzed. When comparing the presence of HPV16 DNA in tumor, metastatic, and normal tissue by ISH, perfect correlation is found at all subsites (P < .0001). However, active infections determined by HPV16 E6 and E7 expression using quantitative polymerase chain reaction or p16 detection by IHC, were present only in primary and metastatic tissue (P = .0012, E6; P = .02, E7). No such correlation was found in normal tissue when compared to primary or metastatic tissue. CONCLUSIONS: There is a clear pattern of active HPV expression that correlates to disease course. In HPV-positive patients, all sites including primary, metastatic, and normal tissues are DNA positive. Transcriptionally active infections were detected in primary and metastatic tissues, whereas normal tissues appear to have latent infections.

LSINCT5 is over expressed in breast and ovarian cancer and affects cellular proliferation.

More than 98% of the human genome is comprised of non-protein coding sequences. Interestingly, a considerable fraction of these sequences is transcribed into non-protein coding RNA transcripts. These transcripts range in size from very small RNAs such as the miRNAs (20-25 base pairs) to transcripts that can range up to 100 kb or more. Some longer non-coding RNAs (lncRNAs) have been found to play important regulatory roles within cells. In this report, we demonstrate that LSINCT5 is a 2.6 Kb polyadenylated, long stress-induced non-coding transcript that is on the negative strand, localized in the nucleus and potentially transcribed by RNA polymerase III. LSINCT5 is overexpressed in breast and ovarian cancer cell lines and tumor tissues, relative to their normal counterpart. In addition, knocking down the expression of LSINCT5 in cancer-derived cell lines causes a decrease in cellular proliferation. Finally, we identified 95 genes with more than 2-fold changes when knocking down LSINCT5 expression by using the Affymetrix U133 Plus 2 array. We chose a subset of these genes to validate using qPCR and found that ten of these genes were indeed significantly affected by the LSINCT5 knockdown. Interestingly, two genes that were significantly downregulated were the lncRNA NEAT-1 and a protein coding gene PSPC1. We have therefore characterized a novel lncRNA that is overexpressed in breast and ovarian cancers, enhances cellular proliferation and may play a significant role in multiple processes.