Changing the Game: The Emergence of NIL Contracts in Collegiate Athletics and the Continued Efficacy of Title IX

On June 30, 2021, the National Collegiate Athletic Association (“NCAA”) suspended a 115-year prohibition on college athletes’ ability to profit from the use of their names, images, and likenesses (“NIL”). Historically, NCAA eligibility was determined by an athlete’s amateur status. Student athletes forewent compensation to preserve a line between professional and college sports. Today, the NCAA’s novel NIL policy recognizes an athlete’s right to publicity and allows them to share in the billions of dollars it generates every year. According to estimates, college athletes earned $917 million in the first year of NIL activity. By 2023, the NIL market is projected to reach$1.14 billion. Despite the abundance of NIL options in the United States, not all athletes benefit. Currently, male athletes receive approximately 74.35% of all NIL compensation. Football and men’s basketball, in particular, receive nearly 71.4% of all NIL deals and 93% of NIL donations. Growth in economic disparity between male and female athletes raises a novel legal question: what role will Title IX, a federal civil rights law enacted to ensure gender equality, play in the NIL era of college sports? This Note analyzes whether Title IX regulations will influence colleges’ and universities’ marketing, promotion, and facilitation of NIL opportunities. In the absence of Title IX’s guarantees of equal access to NIL deals or profits, this Note proposes what could be done to ensure that all public-school students are empowered and uplifted in their pursuit of equitable educational and athletic opportunities

Changes in fruit and vegetable consumption in relation to changes in sleep characteristics over a 3-month period among young adults

OBJECTIVE: To evaluate whether increases in fruit and vegetable (FV) consumption were associated with concomitant changes in insomnia symptoms, sleep duration, and quality. DESIGN: Secondary longitudinal analysis of a randomized trial, baseline to 3 months. SETTING: Integrated health care systems in Detroit, Michigan and Danville, Pennsylvania. PARTICIPANTS: About 1165 young adults who were low consumers of FV (/day) at baseline. INTERVENTION: Online 3-arm program designed to increase FV consumption. MEASUREMENTS: We categorized FV changes into 4 categories: no change or decrease, 1 serving increase, 2 serving increase, and 3 or more serving increase. We then compared the changes in chronic insomnia classification (yes or no), sleep duration, quality, and time to fall asleep (all self-reported) across the FV change categories. Analyses were both overall and stratified by gender, adjusting for potential confounders (depression, physical activity, education, children, and study site). RESULTS: Average age ± SD was 26 ± 2.8 years (71% women). At 3-month follow-up, participants on average increased FV intake by 1.2 ± 1.4 servings. Women who increased FV intake by 3+ servings showed improvements in insomnia symptoms (2-fold higher odds of improvement; 95% CI 1.1 to 3.6), sleep quality (0.2-point higher sleep quality score; 95% CI -0.01, 0.3), and time to fall asleep (4.2 minutes; 95% CI -8, 0) compared to women who did not change or decreased their FV intake. Associations were not as apparent among men. CONCLUSION: Young women with low consumption of FV may experience improvements in insomnia-related sleep difficulties by increasing their consumption of FV

The bHLH transcription factor Mist1 is required to maintain exocrine pancreas cell organization and acinar cell identity

The pancreas is a complex organ that consists of separate endocrine and exocrine cell compartments. Although great strides have been made in identifying regulatory factors responsible for endocrine pancreas formation, the molecular regulatory circuits that control exocrine pancreas properties are just beginning to be elucidated. In an effort to identify genes involved in exocrine pancreas function, we have examined Mist1, a basic helix-loop-helix transcription factor expressed in pancreatic acinar cells. Mist1-null (Mist1KO) mice exhibit extensive disorganization of exocrine tissue and intracellular enzyme activation. The exocrine disorganization is accompanied by increases in p8, RegI/PSP, and PAP1/RegIII gene expression, mimicking the molecular changes observed in pancreatic injury. By 12 m, Mist1KO mice develop lesions that contain cells coexpressing acinar and duct cell markers. Analysis of the factors involved in cholecystokinin (CCK) signaling reveal inappropriate levels of the CCK receptor A and the inositol-1,4,5-trisphosphate receptor 3, suggesting that a functional defect exists in the regulated exocytosis pathway of Mist1KO mice. Based on these observations, we propose that Mist1KO mice represent a new genetic model for chronic pancreas injury and that the Mist1 protein serves as a key regulator of acinar cell function, stability, and identity

Maintenance of Weight Loss in Adolescents: Current Status and Future Directions

There is a dearth of research on the long-term efficacy and safety of treatments for adolescent obesity. This narrative review examined several approaches to treatment, focusing on long-term effectiveness data in adolescents, as well as relevant findings from studies of adults. The available research suggests that lifestyle modification has promise in obese adolescents, although it is not clear that any particular dietary or physical activity approach is more effective than another. Meal replacements are quite effective in adults and deserve further research in adolescents. Extending the length of treatment to teach weight loss maintenance skills is likely to improve long-term outcomes in adolescents, and delivering treatment via the Internet or telephone is a novel way of doing so. Treatment that combines lifestyle modification with the medication orlistat generally appears to be safe but only marginally superior to lifestyle modification alone. More research is needed on the management of adolescent obesity, which has been overlooked when compared with research on the treatment of obesity in children and adults

Single-institution comparative study on the outcomes of salvage cryotherapy versus salvage robotic prostatectomy for radio-resistant prostate cancer

Background Although primary treatment of localized prostate cancer provides excellent oncologic control, some men who chose radiotherapy experience a recurrence of disease. There is no consensus on the most appropriate management of these patients after radiotherapy failure. In this single-institution review, we compare our oncologic outcome and toxicity between salvage prostatectomy and cryotherapy treatments. Methods From January 2004 to June 2013, a total of 23 salvage procedures were performed. Six of those patients underwent salvage prostatectomy while 17 underwent salvage cryotherapy by two high-volume fellowship-trained urologists. Patients being considered for salvage therapy had localized disease at presentation, a prostate-specific antigen (PSA) 10 years at recurrence, and a negative metastatic workup. Patients were followed to observe cancer progression and toxicity of treatment. Results Patients who underwent salvage cryotherapy were statistically older with a higher incidence of hypertension than our salvage prostatectomy cohort. With a mean follow up of 14.1 months and 7.2 months, the incidence of disease progression was 23.5% and 16.7% after salvage cryotherapy and prostatectomy, respectively. The overall complication rate was also 23.5% versus 16.7%, with the most frequent complication after salvage cryotherapy being urethral stricture and after salvage prostatectomy being severe urinary incontinence. There were no rectal injuries with salvage prostatectomy and one rectourethral fistula in the cohort after salvage cryotherapy. Conclusion While recurrences from primary radiotherapy for prostate cancer do occur, there is no consensus on its management. In our experience, salvage procedures were generally safe and effective. Both salvage cryotherapy and salvage prostatectomy allow for adequate cancer control with minimal toxicity

Expression and Mutational Analysis of c-kit in Ovarian Surface Epithelial Tumors

Coexpression of Kit ligand and c-kit has been reported in some gynecologic tumors. To determine whether imatinib mesylate is useful in ovarian epithelial tumors, we performed immunohistochemical and mutational analysis. The cases consisted of 33 cases, which included 13 serous cystadenocarcinomas, 1 borderline serous tumor, 8 mucinous cystadenocarcinomas, 6 borderline mucinous tumors and 5 clear cell carcinomas. Five cases of serous cystadenoma and 5 cases of mucinous cystadenoma were also included. In the immunohistochemical study, 3 cases (3/6, 50%) of borderline mucinous cystic tumor and two cases (2/8, 25%) of mucinous cystadenocarcinoma show positive staining for KIT protein. Only one case (1/13, 7.7%) of serous cystadenocarcinoma had positive staining. On mutational analysis, no mutation was identified at exon 11. However, two cases of borderline mucinous tumors and one case of mucinous cystadenocarcinoma had mutations at exon 17. In these cases, the immunohistochemistry also shows focal positive staining at epithelial component. Although, KIT protein expression showed higher incidence in mucinous tumors than serous tumors, they lack KIT-activating mutations in exon 11. Thus, ovarian surface epithelial tumors are unlikely to respond to imatinib mesylate

An epigenetic reprogramming strategy to re-sensitize radioresistant prostate cancer cells

Radiotherapy is a mainstay of curative prostate cancer treatment, but risks of recurrence after treatment remain significant in locally advanced disease. Given that tumor relapse can be attributed to a population of cancer stem cells (CSC) that survives radiotherapy, analysis of this cell population might illuminate tactics to personalize treatment. However, this direction remains challenging given the plastic nature of prostate cancers following treatment. We show here that irradiating prostate cancer cells stimulates a durable upregulation of stem cell markers that epigenetically reprogram these cells. In both tumorigenic and radioresistant cell populations, a phenotypic switch occurred during a course of radiotherapy that was associated with stable genetic and epigenetic changes. Specifically, we found that irradiation triggered histone H3 methylation at the promoter of the CSC marker aldehyde dehydrogenase 1A1 (ALDH1A1), stimulating its gene transcription. Inhibiting this methylation event triggered apoptosis, promoted radiosensitization, and hindered tumorigenicity of radioresistant prostate cancer cells. Overall, our results suggest that epigenetic therapies may restore the cytotoxic effects of irradiation in radioresistant CSC populations

Transient expression of Ngn3 in Xenopus endoderm promotes early and ectopic development of pancreatic beta and delta cells

Author Posting. © The Author(s), 2011. This is the author's version of the work. It is posted here by permission of John Wiley & Sons for personal use, not for redistribution. The definitive version was published in genesis 50 (2012): 271-285, doi:10.1002/dvg.20828.Promoting ectopic development of pancreatic beta cells from other cell types is one of the strategies being pursued for the treatment of diabetes. To achieve this, a detailed outline of the molecular lineage that operates in pancreatic progenitor cells to generate beta cells over other endocrine cell types is necessary. Here, we demonstrate that early transient expression of the endocrine progenitor bHLH protein Neurogenin 3 (Ngn3) favors the promotion of pancreatic beta and delta cell fates over an alpha cell fate, while later transient expression promotes ectopic development of all three endocrine cell fates. We found that short-term activation of Ngn3 in Xenopus laevis endoderm just after gastrulation was sufficient to promote both early and ectopic development of beta and delta cells. By examining gene expression changes four hours after Ngn3 activation we identified several new downstream targets of Ngn3. We show that several of these are required for the promotion of ectopic beta cells by Ngn3 as well as for normal beta cell development. These results provide new detail regarding the Ngn3 transcriptional network operating in endocrine progenitor cells to specify a beta cell phenotype and should help define new approaches to promote ectopic development of beta cells for diabetes therapy.National Institutes of Health (DK077197