A Clinicopathological Appraisal of Duodenal Neuroendocrine Tumors at a Racially Diverse Safety Net Hospital.

INTRODUCTION: Significant knowledge gaps exist regarding clinicopathological profiling as well as treatment, surveillance, and survival of duodenal neuroendocrine tumors (dNETs). METHODS: We clinicopathologically characterized and identified racial differences among patients with dNETs at a large safety net hospital. Tumor grades were updated based on the World Health Organization 2019 NET classification, and overall survival was determined. RESULTS: We identified 17 dNETs and found no differences in clinicopathologic characteristics across racial groups. Pathological diagnosis was upgraded in 35% of dNETs, and age >65 years significantly shortened overall survival. DISCUSSION: Larger-scale studies are needed to determine the significance of these findings.

Estimate of Increase in Colorectal Cancer Diagnoses with Expansion of Fecal Immunochemical Testing in an Urban Safety-Net Population.

BACKGROUND: Fecal immunochemical test (FIT) is less effective in detecting advanced adenomas (AA) than colonoscopy. Increase in FIT for colorectal cancer (CRC) screening may lead to an increased number of undetected AAs which may develop into future CRCs. AIM: We determined the potential impact of FIT expansion on missed AAs and future CRC diagnoses in an urban, tertiary-care, safety-net hospital. METHODS: CRC and AA diagnoses were identified in patients undergoing colonoscopy for average-risk CRC screening or positive FIT between 2017 and 2019 at Boston Medical Center. Poisson regression modeling was used to estimate the frequency of AAs per year by age group using data from 2017 to 2019, assuming average outpatient volume and proportion of screening colonoscopies. Total number of patients who received FIT was extrapolated from those who underwent colonoscopy for positive FIT. We estimated AAs per year if 'one-time' FIT was used for screening in 75% and 100% of the population and subtracted this from the estimated AAs per year under the Poisson model to determine missed AAs. We used previously described, age and gender specific estimates of the annual progression of AA to CRC. RESULTS: The estimated number of CRCs detected per year is 4.6/1785 males and 4.6/2086 females screened. With 75% FIT expansion, we estimate an additional 3.5 (95% CI 1.3, 9.5) and 2.2 (95% CI 0.64, 7.6) CRCs; with 100% FIT expansion, we estimate an additional 7.4 (95% CI 3.7, 14.9) and 4.2 (95% CI 1.7, 10.5) CRCs, in 5 years, in males and females, respectively. CONCLUSION: Expansion of FIT may substantially increase CRC incidence.

Cardiovascular Complications of Acetylcholinesterase Inhibitors in Patients with Alzheimer's Disease: A Narrative Review.

While acetylcholinesterase inhibitors are used to treat a wide range of patients with Alzheimer's disease, acetylcholinesterase inhibitor use has also been associated with a variety of cardiovascular complications, including bradycardia and syncope. Herein, we review the pathophysiology and clinical evidence for cardiovascular complications caused by acetylcholinesterase inhibitors in patients being treated for dementia and discuss options for their management.

A case of premature ventricular contractions-related cardiomyopathy.

Premature ventricular contractions (PVCs) are heart beats initiated in the ventricles instead of in the sinoatrial node. A high burden of PVCs can lead to a cardiomyopathy, characterised by reduced left ventricular (LV) systolic dysfunction. We present a case of PVC-related cardiomyopathy where the 65-year-old male was initially seen by his primary care provider for recent onset chest pain and dizziness. His transthoracic echocardiogram showed mild concentric LV hypertrophy and mildly reduced systolic function (LV ejection fraction 43%). There was also mild right ventricular (RV) systolic dysfunction. He was started on a beta-blocker and an angiotensin-converting enzyme inhibitor. A 24-hour Holter monitor showed a very high burden of PVCs (32% of all beats). He continued to have frequent PVCs and his echocardiogram did not improve. He was eventually referred for a PVC ablation. Following the ablation, a repeat Holter monitor showed a marked reduction in PVC burden (<1% of beats) and his echocardiogram had normalised.

Hydrogenolysis of ß-O-4 lignin model dimers by a ruthenium-xantphos catalyst.

Hydrogenolysis reactions of so-called lignin model dimers using a Ru-xantphos catalyst are presented (xantphos = 4,5-bis(diphenylphosphino)-9,9-dimethylxanthene). For example, of some nine models studied, the alcohol, 2-(2-methoxyphenoxy)-1-phenylethanol (1), with 5 mol% Ru(H)(2)(CO)(PPh(3))(xantphos) (18) in toluene-d(8) at 135 °C for 20 h under N(2), gives in ~95% yield the C-O cleavage hydrogenolysis products, acetophenone (14) and guaiacol (17), and a small amount (<5%) of the ketone, 2-(2-methoxyphenoxy)-1-phenylethanone (4), as observed by (1)H NMR spectroscopy. The in situ Ru(H)(2)(CO)(PPh(3))(3)/xantphos system gives similar findings, confirming a recent report (J. M. Nichols et al., J. Am. Chem. Soc., 2010, 132, 12554). The active catalyst is formulated 'for convenience' as 'Ru(CO)(xantphos)'. The hydrogenolysis mechanism proceeds by initial dehydrogenation to give the ketone 4, which then undergoes hydrogenolysis of the C-O bond to give 14 and 17. Hydrogenolysis of 4 to 14 and 17 also occurs using the Ru catalyst under 1 atm H(2); in contrast, use of 3-hydroxy-2-(2-methoxyphenoxy)-1-phenyl-1-propanone (7), for example, where the CH(2) of 4 has been changed to CHCH(2)OH, gives a low yield (≤15%) of hydrogenolysis products. Similarly, the diol substrate, 2-(2-methoxyphenoxy)-1-phenyl-1,3-propanediol (9), gives low yields of hydrogenolysis products. These low yields are due to formation of the catalytically inactive complexes Ru(CO)(xantphos)[C(O)C(OC(6)H(4)OMe)=C(Ph)O] (20) and/or Ru(CO)(xantphos)[C(O)CH=C(Ph)O] (21), where the organic fragments result from dehydrogenation of CH(2)OH moieties in 7 and 9. Trace amounts of Ru(CO)(xantphos)(OC(6)H(4)O), a catecholate complex, are isolated from the reaction of 18 with 1. Improved syntheses of 18 and lignin models are also presented.