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ObjectiveDisparities in screening mammography use persists among low income women, even those who are insured, despite the proven mortality benefit. A recent study reported that more than a third of hospitalized women were non-adherent with breast cancer screening. The current study explores prevalence of socio-demographic and clinical variables associated with non-adherence to screening mammography recommendations among hospitalized women.Patients and MethodsA cross sectional bedside survey was conducted to collect socio-demographic and clinical comorbidity data thought to effect breast cancer screening adherence of hospitalized women aged 50–75 years. Logistic regression models were used to assess the association between these factors and non-adherence to screening mammography.ResultsOf 250 enrolled women, 61% were of low income, and 42% reported non-adherence to screening guidelines. After adjustment for socio-demographic and clinical predictors, three variables were found to be independently associated with non-adherence to breast cancer screening: low income (OR = 3.81, 95%CI; 1.84–7.89), current or ex-smoker (OR = 2.29, 95%CI; 1.12–4.67), and history of stroke (OR = 2.83, 95%CI; 1.21–6.60). By contrast, hospitalized women with diabetes were more likely to be compliant with breast cancer screening (OR = 2.70, 95%CI 1.35–5.34).ConclusionBecause hospitalization creates the scenario wherein patients are in close proximity to healthcare resources, at a time when they may be reflecting upon their health status, strategies could be employed to counsel, educate, and motivate these patients towards health maintenance. Capitalizing on this opportunity would involve offering screening during hospitalization for those who are overdue, particularly for those who are at higher risk of disease.

Apolipoprotein synthesis and secretion is upregulated in wallerian degenerating peripheral nerves. A commonly expressed view has been that macrophages are solely responsible for their production. In the present study we provide evidence that (1) nerve‐derived fibroblasts contribute to apolipoprotein production, (2) apolipoprotein production is confined to regions where myelin destruction and phagocytosis occur, and (3) some experimental procedures are detrimental for the production of apolipoproteins. Apolipoprotein production was studied in C57BL/6/NHSD (N) and C57/BL/6‐WLD/OLA/NHSD (W) mice that display, respectively, rapid and slow progression of wallerian degeneration. In N nerves, apolipoprotein E (apo‐E) is produced during in vitro and in vivo degeneration, and in vivo after freeze damage. In W nerves, apo‐E is produced at the injury region where degeneration occurs but not farther distally where degeneration fails to develop. Apo‐E is also produced in W nerves during in vitro degeneration and in vivo after freeze damage. In culture, N and W mice nerve‐derived fibroblasts, but neither macrophages nor Schwann cells produced apo‐E. Two apolipoproteins are produced in in vivo wallerian degenerating and freeze‐damaged frog nerves, i.e., apo‐39 and apo‐29. Only apo‐39 is produced in in vitro degenerating nerves. Neither apo‐39 nor apo‐29 is produced during in vivo degeneration in diffusion chambers. In culture, apo‐39 is produced by nerve‐derived fibroblasts and macrophages but not by Schwann cells.

Collagenous gastritis, without colonic involvement, is exceptionally rare. It is not known to be associated with IgA deficiency and scleroderma. This is the first report of this type of association. We present a 26-year-old white female with a past medical history of gastroesophageal reflux disease and scleroderma. She was evaluated for complaints of abdominal pain and diarrhea. Esophagogastroduodenoscopy showed gastritis and duodenitis. Colonoscopy was normal. The histopathological report showed collagenous gastritis and focal lymphocytic duodenitis. A definitive treatment has not been established for this condition. Reporting such cases furthers understanding of the disease and will help to establish diagnostic criteria and to develop therapeutic strategies.

Background and study aims Guidelines for management of presumed neoplastic pancreatic cysts have encouraged noninvasive imaging for low-risk surveillance, while reserving endoscopic ultrasound for worrisome features including morphologic change. We aim to study the impact of endoscopic ultrasound on diagnosis and management compared with non-invasive imaging. Patients and methods A single-institution pancreatic cyst database was retrospectively queried for patients who underwent endoscopic ultrasound for the indication of change in cyst morphology. Diagnoses were classified as presumed mucinous neoplasm with or without worrisome features or high-risk stigmata and non-mucinous lesions. Management decisions were defined a priori as surgical evaluation for patients with high-risk stigmata, positive cytology or mural nodule, or continued surveillance for all others. Results Between January 2013 and October 2016, 709 pancreas cyst endoscopic ultrasounds were performed of which 89 were for cyst morphology change seen on noninvasive imaging including 10 presumed pseudocysts, nine presumed serous cystadenomas, and 70 presumed mucinous cystic neoplasms. Cyst morphologic changes included increase in caliber of the main pancreatic duct (7 cases), increase in cyst size (68 cases), cyst ≥ 30 mm (10 cases), and presence of a solid nodule (1 case). Median cyst size increase was 5 mm with interquartile range of 4 mm over 2.1 ± 1.9 years. Endoscopic ultrasound done for morphologic change resulted in a change in diagnosis and management in 16 % and 13 % of cases, respectively. Conclusion Endoscopic ultrasound has a modest but clinically significant role in impacting diagnosis and management for presumed mucinous cystic neoplasms when performed for the indication of cyst morphology change.