China
Africa
Explore chapters and articles related to this topic
Effects of Environmental Factors on the Endocrine System
Published in George H. Gass, Harold M. Kaplan, Handbook of Endocrinology, 2020
The endocrine system plays a crucial regulatory role in the internal environment of an organism. Some of its components had evolved to merge with the nervous system that possesses sensory detectors for external stimuli such as light and temperature. This integration of neural and endocrine tissues created a neuroendocrine interface capable of accepting neural signal inputs and secreting hormones into the blood circulation. It can transduce information from the external environment into endocrine signals.1 With the ability to receive and interpret environmental cues through the neuroendocrine system, the endocrine system is enhanced in its adaptability to the environment. In response to external environmental changes, proper endocrine adjustments can be evoked in the internal environment. The neuroendocrine system, as its name implies, is an integrated control system of both neural and endocrine functions. In this chapter, the neuroendocrine system is discussed as a part of the endocrine system, though it can be considered as a system on its own.2
Senescence
Published in Nate F. Cardarelli, The Thymus in Health and Senescence, 2019
In 1922 Gley stated that human aging results from the gradual failure of the endocrine system.123 In Cowdry’s Problems of Aging (1952) Carlson discusses the lack of substantiation for this view.124 Much more recently, it has been shown that providing l-dopamine, a neurotransmitter to swiss albino mice at 40 mg/g mouse weight gives a highly significant increase in longevity125 (50 mg/g is 100% fatal). The relationship between neuroendocrine dysfunction and aging remains of interest to the scientific community.126 Neuroendocrine systems regulate cell growth and differentiation, and loss of function leads to various symptoms associated with advancing age.83,127 The rate of living (metabolism) hypothesis and the neuroendocrine decay hypothesis are related in several ways. For instance, chronic underfeeding leads, through mechanisms unknown, to an increase in dopamine receptors. Levin et al. report that dietarily restricted rats had a 50% increase in dopamine receptors and a 40% increase in longevity.128
Introductory Remarks
Published in Dongyou Liu, Tumors and Cancers, 2017
A tumor/cancer is usually named for the organs or tissues where it starts (e.g., brain cancer, breast cancer, lung cancer, lymphoma, and skin cancer). Depending on the types of tissue involved, tumors/cancers are grouped into a number of broad categories: (i) carcinoma (involving epithelium), (ii) sarcoma (involving soft tissue), (iii) leukemia (involving blood-forming tissue), (iv) lymphoma (involving lymphocytes), (v) myeloma (involving plasma cells), (vi) melanoma (involving melanocytes), (vii) central nervous system cancers (involving brain or spinal cord), (viii) germ cell tumors (involving cells that give rise to sperm or eggs), (ix) neuroendocrine tumors (involving hormone-releasing cells), and (x) carcinoid tumors (a variant of neuroendocrine tumors found mainly in the intestinal tract).
Piflufolastat F-18 (18F-DCFPyL) for PSMA PET imaging in prostate cancer
Published in Expert Review of Anticancer Therapy, 2022
Andrew F. Voter, Rudolf A. Werner, Kenneth J. Pienta, Michael A. Gorin, Martin G. Pomper, Lilja B. Solnes, Steven P. Rowe
The power of molecular imaging, including PSMA-PET, derives from the exquisite precision of the agents in combination with their modularity. While 18F-DCFPyL is exclusively an imaging agent, different warheads can be loaded onto the PSMA inhibitor delivery vehicle to address a range of clinical scenarios. This approach has been validated in neuroendocrine tumors. Somatostatin receptor PET/CT with 68Ga-labelled somatostatin analogues rapidly replaced 111In-based somatostatin receptor scintigraphy scans for imaging and staging of neuroendocrine tumors [108]. However, replacement of the gallium-68 PET imaging radionuclide with a lutetium-177 warhead yielded a therapeutic agent that has revolutionized the treatment of carcinoid tumors [109]. Similar efforts are underway for the PSMA agents, with initial trials showing favorable results for the treatment of metastatic castration-resistant prostate cancer [110–112]. The VISION trial, a prospective, phase III randomized trial, demonstrated that men with metastatic castration-resistant, PSMA-positive prostate cancer who were treated with 177Lu-PSMA-617 in addition to standard of care therapies had a significantly increased overall survival. This led to the FDA approval of 177Lu-PSMA-617 for use in this population in 2022 [113]. Further trials to explore the potential role of this agent earlier in the disease course are currently underway.
Early esophageal neuroendocrine tumor
Published in Baylor University Medical Center Proceedings, 2022
Heather Branstetter, Atin Agarwal, Scott Paulson, Anh D. Nguyen, Vani Konda
The histology from the EMR specimen demonstrated a 1 mm tumor with cells in both nest and rosette pattern extending into the muscularis mucosa (Figure 2). The cells were positive for chromogranin, synaptophysin, and cytokeratin on immunohistochemical staining. Additionally, Ki-67 was <2%. These histologic findings were consistent with a well-differentiated neuroendocrine tumor. There were negative margins on the resected specimen, and a computed tomography scan showed no evidence of metastatic disease. Oncology concluded that the tumor was a primary distal esophageal neuroendocrine tumor that was completely resected by EMR with negative margins. The rest of the biopsy specimens obtained with a mapping protocol were consistent with Barrett’s esophagus, with focal low-grade dysplasia but no evidence of high-grade dysplasia or esophageal adenocarcinoma. The patient completed endotherapy and is in her second year of surveillance without evidence of recurrence of either dysplasia or tumor.
Sepsis-associated encephalopathy and septic encephalitis: an update
Published in Expert Review of Anti-infective Therapy, 2021
Simone C. Tauber, Marija Djukic, Johannes Gossner, Helmut Eiffert, Wolfgang Brück, Roland Nau
The pathophysiology of SAE still is incompletely understood. The immune privilege of the CNS depends on the morphological architecture of its borders resembling a medieval castle. The blood-brain barrier (BBB) and blood-CSF barrier serve as the outer walls of the castle [45]. The brain senses a septic infection under physiological conditions by several ways: (a) leaky regions of the BBB barrier in the circumventricular organs (CVOs) comprising approximately 1:5000 of the entire capillary surface area, (b) afferent fibers of several nerves, particularly of the vagus nerve, and c) direct communication across the BBB [46]. The brain has an important role in the regulation of the immune system, particularly via the neuroendocrine network. The main abnormalities in sepsis comprise (a) dysfunction of the neuroendocrine network, (b) diffuse neuroinflammation with BBB leakage and inflammation-induced damage to neurons and glial cells, (c) impaired circulation leading to impaired autoregulation and ischemia, and (d) imbalance of neurotransmitters leading to excitotoxicity [11,14] (Figure 1). These four major pathophysiologic mechanisms are discussed in detail below.