Citations

We determined if changes in the irregular motor activity of phase II, the dominant motility phase in awake fasting humans, are associated with fluctuations in pancreatic secretion by intubating the upper gastrointestinal tract of 15 healthy humans and recording antral and duodenal motility and obtaining duodenal samples for one or two interdigestive motility cycles. Antral phase II activity was graded as having low, intermediate, or high frequency of contractions and related to duodenal trypsin output and plasma concentrations of motilin and human pancreatic polypeptide (HPP), a marker of vagal cholinergic tone. Low, intermediate, and high phase II motor activities were significantly associated with trypsin outputs (U/10 min; mean +/- SE) of 576 +/- 137, 1,441 +/- 225, and 3,621 +/- 521, respectively (P less than 0.001). Plasma motilin levels did not vary with the grades of phase II motility (P greater than 0.1), but levels of plasma HPP and the grades of phase II motility were positively correlated (P less than 0.001). The close correlation among motility, pancreatic secretion, and plasma HPP during phase II suggests that vagal cholinergic pathways are involved in the common regulatory mechanism controlling phase II interdigestive motility and pancreatic secretion.

We tested the hypothesis that the duodenum is necessary to coordinate interdigestive pancreatic trypsin secretion with gastrointestinal motility and determined whether duodenectomy altered interdigestive cycles of plasma motilin and pancreatic polypeptide and their relationship to trypsin secretion and motility. Consequently, in normal and duodenectomized dogs, we measured trypsin secretion, gastrointestinal motility, and plasma concentrations of motilin and pancreatic polypeptide during the interdigestive period. After duodenectomy, peaks of trypsin secretion continued to cycle at normal intervals (102 +/- 15 min), but the amounts of trypsin were reduced during peaks of secretion (P = 0.02) and throughout the entire cycle (P = 0.02). Trypsin secretory cycles after duodenectomy, however, were not coordinated with cycles of interdigestive motility, and the plasma concentrations of motilin (P = 0.02) and pancreatic polypeptide (P = 0.05) were reduced and had no cyclic pattern. In addition, we confirmed that duodenectomy alters canine interdigestive antral motility, interrupts coordination between antral and intestinal motility, and shortens the period of jejunal migrating motor complexes. We conclude that duodenectomy disrupts the relationship between the cycles of interdigestive gastrointestinal motility and trypsin secretion and reduces the amount of interdigestive trypsin secretion. These effects of duodenectomy may be due to interruption of the duodenopancreatic neural connections or the hormonal abnormalities we have described. The loss of the cyclic pattern of plasma pancreatic polypeptide after duodenectomy suggests that the duodenum controls the release of pancreatic polypeptide by either a neural or hormonal mechanism.

To determine if human lipase is inactivated by trypsin and chymotrypsin, we intubated 22 human subjects with an oroduodenal tube and stimulated pancreatic secretion with cholecystokinin octapeptide. The duodenal aspirate from each subject was divided into a control and a test sample and incubated in a 37 degrees C water bath for 2 h. An inhibitor of trypsin or chymotrypsin or more of one of these enzymes was added to the test sample. We found that the loss of lipase activity was partly prevented by inhibiting trypsin with aprotinin (910 KU/ml; P = 0.03) and was accelerated by adding bovine trypsin (2.5 mg/ml; P = 0.01). Inhibiting chymotrypsin with turkey egg white (2.5 mg/ml) totally abolished the loss of lipase activity (P = 0.01), and addition of bovine chymotrypsin (5 mg/ml) accelerated the loss of lipase activity more than adding trypsin (P = 0.01). After inhibiting chymotrypsin (to maintain lipase activity), increasing trypsin activity by adding a single or repeated doses of trypsin did not decrease lipase activity. Conversely, the addition of a single dose of chymotrypsin after inhibiting trypsin activity markedly decreased lipase activity (P less than 0.004). In conclusion, chymotrypsin is a more potent inactivator of human lipase than trypsin; chymotrypsin inactivates lipase in the absence of trypsin, but trypsin inactivation of lipase requires chymotrypsin.

Increasing rates of burnout—with accompanying stress and lack of engagement—among faculty, residents, students, and practicing physicians have caused alarm in academic medicine. Central to the debate among academic medicine’s stakeholders are oft-competing issues of social accountability; cost containment; effectiveness of academic medicine’s institutions; faculty recruitment, retention, and satisfaction; increasing expectations for faculty; and mission-based productivity. The authors propose that understanding and fostering what contributes to faculty and institutional vitality is central to preventing burnout during times of change. They first look at faculty vitality and how it is threatened by burnout, to provide a framework for a greater understanding of faculty well-being. Then they draw on higher education literature to determine how vitality is defined in academic settings and what factors affect faculty vitality within the context of academic medicine. Next, they propose a model to explain and examine faculty vitality in academic medicine, followed by a discussion of the need for a greater understanding of faculty vitality. Finally, the authors offer conclusions and propose future directions to promote faculty vitality. The authors encourage institutional decision makers and other stakeholders to focus particular attention on the evolving expectations for faculty, the risk of extensive faculty burnout, and the opportunity to reduce burnout by improving the vitality and resilience of these talented and crucial contributors. Faculty vitality, as defined by the institution, has a critical role in ensuring future institutional successes and the capacity for faculty to thrive in a complex health care economy.

OPLAH is cardioprotective for myocardial infarction, and its substrate 5-oxoproline is a putative circulating marker for heart failure.

Abstract Introduction: The endocannabinoid system (ECS) regulates functions throughout human physiology, including neuropsychiatric, cardiovascular, autonomic, metabolic, and inflammatory states. The complex cellular interactions regulated by the ECS suggest a potential for vascular disease and stroke prevention by augmenting central nervous and immune cell endocannabinoid signaling. Discussion: The endocannabinoid N-arachidonoylethanolamine (anandamide) plays a central role in augmenting these processes in cerebrovascular and neurometabolic disease. Furthermore, cannabidiol (CBD), a nonpsychoactive constituent of Cannabis , is an immediate therapeutic candidate both for potentiating endocannabinoid signaling and for acting at multiple pharmacological targets. Conclusion: This speculative synthesis explores the current state of knowledge of the ECS and suggests CBD as a therapeutic candidate for stroke prevention by exerting favorable augmentation of the homeostatic effects of the ECS and, in turn, improving the metabolic syndrome, while simultaneously stalling the development of atherosclerosis.

Schwannomas are benign soft-tissue tumors that arise from peripheral nerve sheaths throughout the body and are commonly encountered in patients with neurofibromatosis Type 2. The vast majority of schwannomas are benign, with rare cases of malignant transformation reported. In this pictorial review, we discuss the magnetic resonance imaging (MRI) appearance of schwannomas by demonstrating a collection of tumors from different parts of the body that exhibit similar MRI characteristics. We review strategies to distinguish schwannomas from malignant soft-tissue tumors while exploring the anatomic and histologic origins of these tumors to discuss how this correlates with their imaging findings. Familiarity with the MRI appearance of schwannomas can help aid in the differential diagnosis of soft-tissue masses, especially in unexpected locations.