Abstract. Background: Obesity is an established risk factor for the development of pancreatic ductal adenocarcinoma (PDACPancreatic ductal adenocarcinoma (PDAC) carries an extremely poor prognosis, with a 5-year survival rate of less than 6% in the United States (1). The low survival rate is due to the late stage at which patients are usually diagnosed, with only 20% of patients being eligible for tumor resection at the time of diagnosis (1). Several risk factors for PDAC are firmly established, such as chronic pancreatitis (2), cigarette smoking (3), family history of pancreatic cancer (4), and diabetes mellitus (5).Both epidemiological and experimental studies have also linked obesity to the development of PDAC. In a large casecontrol study, Silverman et al. (6) showed obesity portends a 50-60% increased risk of PDAC in both men and women. Similarly, a pooled case-control analysis using data from the Pancreatic Cancer Cohort Consortium (PanScan) comparing 2170 PDAC cases to 2209 controls showed a positive association between increasing body mass index (BMI) and risk of PDAC [adjusted odds ratio (aOR) for the highest vs. lowest BMI quartile=1.33, 95% confidence interval (CI)= 1.12-1.58, p<0.001 (7).The mechanism of how obesity increases PDAC risk is poorly understood. Previous studies have shown that increased peritumoral fat density promotes metastasis and increases mortality in patients with PDAC (8). Adipose triglyceride lipase (ATGL) is a lipase in adipose tissue that catabolizes the first step in triglyceride hydrolysis and is responsible for the release of free fatty acids. Another lipase called monoacylglycerol lipase has been shown to be overexpressed in human cancer cell lines and to promote in vivo tumor growth via 'feeding' cancer cells with free fatty acids (9). Previous studies of breast cancer demonstrated increased peritumoral ATGL expression in fat cells of obese 699 Τhis article is freely accessible online.

Langerhans cell histiocytosis (LCH) is a proliferative disorder of Langerhans cells that can be challenging to distinguish histologically from Langerhans cell (LC) hyperplasia, seen in a variety of inflammatory dermatoses. Lesional cells in both entities demonstrate positive staining for CD1a and S100. Previous studies have demonstrated positive staining of fascin, CD31, and p53 in cases of LCH, but currently, no studies have compared the staining profiles of these markers between LCH and LC hyperplasia. The authors compared immunohistochemical staining profiles of LCH (n = 15) and various inflammatory dermatoses with LC hyperplasia (n = 15) using fascin, CD31, and p53. Fascin, CD31, and p53 were graded as a percentage of CD1a staining cells in the epidermis and dermis of each specimen. Fascin showed no significant differences in staining between the 2 entities. CD31 was positive in the dermal infiltrate in 40% of cases of LCH and negative in all cases of LC hyperplasia. p53 was positive in the epidermal infiltrate in 50% of cases of LCH, and positive in the dermal infiltrate in 93% of cases of LCH, whereas negative in all cases of LC hyperplasia. Fascin was not a helpful marker in distinguishing LCH from LC hyperplasia. CD31, if positive in the dermal infiltrate, is suggestive of a diagnosis of LCH, but exhibits a relatively low sensitivity for this purpose. p53 proved to be a helpful and accurate diagnostic immunohistochemical stain when distinguishing between LCH and LC hyperplasia.

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Objectives Identify which delivery modality for skin reconstruction care, face‐to‐face (FTF) in‐person versus two telemedicine modalities, store‐and‐forward (S&F) and live video chat (LVC), is patient preferred and how cost, access, wait time, and demographics influence this preference. Study Design Cross‐sectional survey. Methods A 16‐question survey querying demographics and five scenario‐specific preferences questions for the delivery of skin cancer reconstruction care was created and distributed via Amazon Mechanical Turk (MTurk), a crowdsourcing online marketplace, and in‐person to Mohs micrographic surgery patients. Results 1394 MTurk and 55 in‐person responses were included. While 82.1% of online respondents prefer FTF clinic visits, this decreases to 58.3% with an in‐person visit cost (p < 0.01) and furthermore to a minority 43.5% with both an in‐person visit cost and wait time (p < 0.01) despite 77.8% believing that usefulness to the surgeon would improve FTF. Both the MTurk and in‐person cohorts demonstrated similar response patterns despite considerable demographic differences. Multivariable analyses revealed that telemedicine was preferred by MTurk respondents with Medicaid (adjusted OR [95% CI]: 1.97 [1.18–3.31]) or Medicare (1.69 [1.10–2.59]) versus private insurance, and prior skin cancer (2.01 [1.18–3.42]) and less preferred by those earning $140,000+ per year (0.49 [0.29–0.82]) compared to those earning <$20,000 per year. Conclusions FTF visits are preferred for skin cancer reconstruction care; this shifts toward virtual care with a cost and wait time in spite of the perceived quality of care. Individuals with socioeconomic barriers to access prefer telemedicine. MTurk can be a valuable tool for behavioral research in FPRS. Level of Evidence NA Laryngoscope, 133:294–301, 2023

Background:Telogen effluvium (TE) is a type of acquired, diffuse alopecia that occurs due to an abnormal shift of scalp hair follicles from anagen to telogen, leading to premature shedding of hair. Previous studies have suggested the existence of a neuroimmunologic “brain-hair follicle” axis, in which mast cells have been implicated as an important link between the nervous system and immunologic system.Objective:The current study sought to investigate the role of mast cell presence and mast cell degranulation in the pathogenesis of TE.Materials and Methods:Mast cells were counted using Giemsa and tryptase immunohistochemical stains in scalp biopsy specimens with the pathologic diagnosis of TE (TE, n = 10), alopecia areata (AA, n = 7), and androgenic alopecia (ANDRO, n = 9).Results:We found significant (P < 0.001) group-level differences between the mean mast cell counts per high-power fields for each type of alopecia studied. Tukey post hoc analysis showed the mean mast cell count for TE to be significantly larger than AA for both Giemsa (P = 0.002) and tryptase (P = 0.006); significantly larger than ANDRO for both Giemsa (P < 0.001) and tryptase (P < 0.001); and significantly larger when compared to normal scalp skin for both Giemsa (P < 0.001) and tryptase (P < 0.001). No significant difference of mean mast cell counts was observed for AA compared to ANDRO for Giemsa (P = 0.373) or tryptase (P = 0.598) stains.Conclusion:Our findings suggest that mast cells could play a role in mediating stress-induced hair loss seen in TE.