In the olfactory epithelium (OE), generation of new neurons by neuronal progenitors is inhibited by a signal from neurons themselves. Here we provide evidence that this feedback inhibitory signal is growth and differentiation factor 11 (GDF11). Both GDF11 and its receptors are expressed by OE neurons and progenitors, and GDF11 inhibits OE neurogenesis in vitro by inducing p27(Kip1) and reversible cell cycle arrest in progenitors. Mice lacking functional GDF11 have more progenitors and neurons in the OE, whereas mice lacking follistatin, a GDF11 antagonist, show dramatically decreased neurogenesis. This negative autoregulatory action of GDF11 is strikingly like that of its homolog, GDF8/myostatin, in skeletal muscle, suggesting that similar strategies establish and maintain proper cell number during neural and muscular development.
After completing this course, the reader will be able to:1. Identify the components of the "postembolization syndrome": elevated liver function tests, right upper quadrant pain, nausea and vomiting, and fever.2. Distinguish the postembolization syndrome from rare complications of embolization that would merit an extended hospitalization.This article is available for continuing medical education credit at CME.TheOncologist.com. CME CME
ABSTRACTBackground. There is scant evidence to guide the management of patients after hepatic artery embolization (HAE). We examined length of stay (LOS), laboratory patterns, medication usage, morbidity, and mortality of patients hospitalized after HAE for metastatic neuroendocrine tumors. Methods. Data were abstracted retrospectively from electronic medical records on LOS, liver function tests (LFTs), i.v. antibiotics, analgesia, peak temperature, bacteremia, hepatic abscess formation, carcinoid crisis, and metastatic burden on cross-sectional imaging.
Peripheral T-cell lymphomas (PTCL) represent about 12%–15% of non-Hodgkin lymphomas and are characterized for being a molecularly heterogenous group of diseases. The optimal treatment for PTCLs remains to be defined as they are usually refractory to existing therapies and carry a poor prognosis. Pralatrexate (PDX), a rationally designed antifolate drug, was granted FDA approval as a single agent for the treatment of relapsed/refractory PTCL in 2009. Because of its favorable toxicity profile and activity, Pralatrexate has become a major compound for patients with refractory PTCL.
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