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Medicare is a large government health insurance program in the United States that covers about 60 million people. This paper analyzes the effects of Medicare insurance on health for a group of people in urgent need of medical care: people with cancer. We used a regression discontinuity design to assess impacts of near-universal Medicare insurance at age 65 on cancer detection and outcomes, using population-based cancer registries and vital statistics data. Our analysis focused on the three tumor sites for which screening is recommended both before and after age 65: breast, colorectal, and lung cancer. At age 65, cancer detection increased by 72 per 100,000 population among women and 33 per 100,000 population among men; cancer mortality also decreased by nine per 100,000 population for women but did not significantly change for men. In a placebo check, we found no comparable changes at age 65 in Canada. This study provides the first evidence to our knowledge that near-universal access to Medicare at age 65 is associated with improvements in population-level cancer mortality., (© 2020 The Authors. Journal of Policy Analysis and Management published by Wiley Periodicals, Inc. on behalf of Association for Public Policy and Management.)

Objective: To determine whether identification of previously undiagnosed high cholesterol, hypertension, and/or diabetes during an in-home assessment impacts care seeking among Medicare beneficiaries., Data Sources/study Setting: Data from the REasons for Geographic And Racial Differences in Stroke (REGARDS) study, which recruited African American and white participants across the continental United States from 2003-2007, were linked to Medicare claims., Study Design: We used panel data models to analyze changes in doctor visits for evaluation and management of conditions after participants were assessed, utilizing the study's rolling recruitment to control for secular trends., Data Extraction Methods: We extracted Medicare claims for the 24 months before through 24 months after assessment via REGARDS for 5,884 participants., Principal Findings: Semi-annual doctor visits for previously undiagnosed conditions increased by 22 percentage points (95 percent confidence interval: 16-28) 2 years following assessment. The effect was similar by gender, race, region, and Medicaid, but it may have been lower among participants who lacked a usual health care provider., Conclusions: In-home assessment of cholesterol, blood pressure, and blood glucose can increase doctor visits for individuals with previously undiagnosed conditions. However, biomarker assessment may have more limited impact among individuals with low access to care., (© Health Research and Educational Trust.)

Rats were orally administered separately one dose of three labelled long-chain fatty acids: [1-14C] oleic, [1-14C] palmitic or [1-14C] stearic. Samples of lymph were obtained from previously cannulated thoracic ducts and analyzed for the composition and content of labelled fatty acids. Most of the newly recovered and labelled fatty acids were qualitatively and quantitatively similar regardless of which 14C-fatty acid had been administered. Over 20% of the administered fat were interconverted in six hours. The results suggest that the mucosa of the small intestine, the first sites of fatty acid absorption, is also one of the sites of various metabolic processes such as beta oxidation and synthesis which are responsible for some of the changes observed. These processes indicated that by shortening or lengthening the fatty acid composition, the content of the lymph became approximately the same regardless of the precursor fatty acid. The intestinal mucosa became the first tissue to help maintain lipid homeostasis in the rat.

A unique outpatient surveillance program consisting of an initial phase (phase I) and a follow-up phase (phase II) was initiated 7 months after FDA approval of cimetidine. The methodology used in this extensive postmarket surveillance program provided information on adverse effects in a large number of patients both on an acute and chronic (up to 12 months) basis. Phase I gathered data on 9907 patients from 1049 physicians over a 3-month period. The overall incidence of adverse effects in this phase was 4.4%, and they did not differ in type from those of premarketing controlled studies. Six months after termination of phase I, phase II was initiated, and follow-up data were requested on the same group of patients from the same 1049 physicians. Case report forms were received from 905 physicians on 7248 patients representing 9763 courses of cimetidine therapy. A total of 162 adverse effects were reported by 138 patients for an incidence of 1.8%. As in postmarket surveillance I, the adverse effects reported in postmarket surveillance II were not different from those previously reported in clinical studies, published reports, or via the spontaneous reporting system. This postmarket surveillance program designed and successfully tested methodology useful for future surveillance studies, and confirmed the safety of cimetidine in a large cohort of patients which remains a valuable source for future data accumulation.

A postmarket surveillance program in outpatients receiving cimetidine was initiated seven months after its approval for marketing. During the first phase of the program, data were obtained over a three-month period for 9,907 patients who received the drug. The overall incidence of adverse effects reported was 4.4%, and the types of adverse effects did not differ from those reported in premarketing controlled studies. Physician response was excellent (85.1%), and the methods used were successful in providing data on a large number of patients who received the drug in routine clinical practice. The results confirmed the safety profile of cimetidine. A follow-up phase, initiated six months after the initial phase of the surveillance program, will provide longer-term data on these patients.

We describe a new, more efficient, and more reproducible method for determination of octanoate in serum. This method involves ethanol extraction, followed immediately by alkali addition before concentration of the extract. The concentrate is made acidic only before it is to be steam distilled (in a special all-glass apparatus with an alkali trap). The material is acidified again just before separation by gas-liquid chromatography. The yield is 89-107%. When assayed by mass spectrometry, only octanoate was found in the fraction from chromatography. Previous methods yielded only 30-55% of the expected octanoate value and the recovered materials showed impurities by mass spectrometry. Octanoate concentrations were determined in the serum of 24 fasting controls and that of 85 fasting cirrhotic patients, of whom 50 had encephalopathy. Concentrations in arterial and venous blood were significantly higher in cirrhotic patients in coma than in those not in coma, and arterial concentrations were statistically higher than venous concentrations in the cirrhotic patients.

Serum octanoate levels of patients with liver cirrhosis and hepatic encephalopathy have been shown to be three to 15 times higher than those of controls. Assays for octanoate have been modified to permit isolation of pure octanoate after GLC. Patients with these conditions were given intravenously differently labeled [14C]-palmitates; serum [14C]-octanoate was isolated in each case and shown by mass spectrometry to be authentic octanoate. [1-14C]-oleate and [1-14C]-stereate were also shown to serve as precursors of serum [14C]-octanoate. When differently labeled palmitates (1-[14C]; omega [14C]; and [14C]-uniformly labeled) were used, different yields of serum [14C]-octanoate were recovered. Octanoate samples were chemically degraded to yield individual carbons or groups of carbons. In this manner it was possible to determine the percentage distribution of the [14C] label within the octanoate carbon chain. The data obtained from these studies suggest that 60% to 80% of the serum octanoate was obtained from the incomplete beta-oxidation of long-chain fatty acids and that 20% to 40% of the octanoate may have been formed de novo.

A new and sensitive method for determination of octanoate in serum by gas-liquid chromatography is described. It was validated by mass spectrometry. Octanoate concentrations were determined in the serum of 61 fasting cirrhotic patients of which 47 also had hepatic encephalopathy. Concentrations in arterial and venous blood were higher in cirrhotic patients with encephalopathy than in those without and higher in the latter than in controls. Arterial concentrations were higher than venous concentrations and octanoate and ammonia varied independently. A predominant endogenous origin is likely. Data obtained from studies using palmitic acid labeled at different loci suggest that recovered serum octanoate was formed mostly by incomplete oxidation of long chain fatty acids. Sodium octanoate infusion to rhesus monkeys studied polygraphically induces a temporary coma.