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Associated Methods
Published in Lars-Inge Larsson, Immunocytochemistry: Theory and Practice, 2020
I believe that the techniques for studying ligand binding to fixed tissue sections by immunocytochemistry will never be universally accepted. Thus, as already stated, kinetic parameters cannot readily be obtained. Much unspecific binding of ligands will occur in most situations and enzymes, binding proteins, and other unspecific factors all will operate. Evidence for binding of gastrin-releasing peptide [14-27] to hypothalamic magnocellular neurons has been presented and considered to be due to binding to neurophysin.80 Moreover, if a real interaction takes place, it is reasonable to assume that part of the ligand structure will become masked by the receptor protein. This was directly shown for the a subunit of human chorionic gonadotropin.74 Therefore, most antibodies would be unable to detect the ligand-receptor complex. This was realized by Lackie et al.59 who employed a dimeric ligand for studying bombesin receptors on small cell carcinoma cells of lung. In this study, Lys3-bombesin was dimerized by glutaraldehyde. It was felt that one part of the dimer would interact with the receptor on live cultured cells and that the other part would be free to interact with a monoclonal bombesin antibody which subsequently was detected by indirect immunogold staining.59 Staining of cells was obtained and could be competed for by monomeric bombesin.59 The biological activity of the bombesin dimer was not given.
An Overview of the Biological Actions and Neuroendocrine Regulation of Growth Hormone
Published in George H. Gass, Harold M. Kaplan, Handbook of Endocrinology, 2020
Bombesin was initially isolated from amphibian skin222 and later reported to be present in mammalian brain.223 Bombesin is a tetradecapeptide, and its role as a central nervous system neurotransmitter is currently under investigation. Early studies indicated that both intravenous and intracisternal administration of bombesin to steroid-primed male rats produced a considerable rise in plasma growth hormone, although intravenous injection was more effective. However, more recent studies suggest that intracerebroventricular administration of the peptide inhibits both growth hormone secretion and the response to opioid stimulation, possibly as a result of increased somatostatin secretion.224 A possible confounding factor in several studies of the effects of bombesin (as well as other compounds) is that bombesin can increase growth hormone secretion from pituitary cells.225,226
Gastroenteropancreatic Regulatory Peptide Structures: An Overview
Published in Edwin E. Daniel, Neuropeptide Function in the Gastrointestinal Tract, 2019
In the mammal, GRP appears to be confined strictly to neural elements of the central, peripheral, and enteric nervous systems, with the exceptions that it is also found in neuroendocrine cells of the peribronchial epithelium and in neuroendocrine cells present in small cell lung cancer, medullary carcinoma of the thyroid, and carcinoid tumors. Intracerebral administration of GRP to mammals results in potent and diverse biological effects, including the production of hypothermia, hyperglycemia, altered satiety mechanisms, and increased sympathetic tract outflow. Peripheral i.v. administration of GRP potently effects the release of a number of biologically active peptides (hormones, neuropeptides), alters gastrointestinal smooth muscle activity, and has potent effects on the exocrine secretion of the pancreas and stomach. Although no single biological function of GRP or bombesin has been demonstrated to be physiological, strong suggestive evidence has been reported for a role for GRP in vagal mechanisms resulting in the release of gastrin from endocrine cells in the gastric antrum. The bombesin-like peptides also have putative trophic roles in the lung, gastric antrum, and pancreas and have been implicated as autocrine growth factors in human small cell lung cancer.309 The role of bombesin-like peptides in health and disease has recently been the subject of an international symposium307 and has been the subject of recent reviews.292,310
Predicting the likelihood of bronchopulmonary dysplasia in premature neonates
Published in Expert Review of Respiratory Medicine, 2019
Patrick A Philpot, Vineet Bhandari
Urine metabolites and have recently been identified in preterm infants who develop BPD. Bombesin-like peptide is produced by neuroendocrine cells in the lung and increased levels precede BPD. Cullen et al. evaluated 132 infants ≤28 weeks GA and analyzed bombesin-like peptide levels over the first 4 days of life and compared it in infants who developed BPD with those who did not [33]. A first urine bombesin-like peptide level greater than 20,000 pg/mg creatinine (12,500 fmol/mg) between postnatal days 1–4 occurred among 54% of the infants who developed BPD (p ≤ 0.001), versus 10% among non-BPD infants (specificity 90%). Multivariable logistic regression analyses revealed that elevated urine bombesin-like peptide levels were associated with BPD (OR 9.9, 95% CI 3.4, 29) (p ≤ 0.001). The authors concluded that elevated bombesin-like peptide levels at 1–4 days after birth are associated with a 10-fold increased risk of developing BPD.
Chronic interstitial lung diseases in children: diagnosis approaches
Published in Expert Review of Respiratory Medicine, 2018
Nadia Nathan, Laura Berdah, Keren Borensztajn, Annick Clement
Neuroendocrine cell hyperplasia of infancy (NEHI) is a non-lethal disease characterized by a tachypnea without respiratory failure in very young infants. The human airway epithelium contains highly specialized pulmonary neuroendocrine cells. These cells are the first specialized epithelial cells to appear in the lung. Their function remains unknown but is hypothysed to act as mechano and chemo-sensors and to secrete amines and vasopeptides such as gastrin-releasing peptide (GRP) or bombesin. As normal bombesin level decreases after mid-gestation, its overexpression in NEHI could be attributed to a non-regression of neuroendocrine cells. Some molecular defects have recently been documented [53–55]. Clinical presentation is typically a respiratory distress with tachypnea that usually evolves spontaneously well [56]. Pseudo-asthmatic presentations have been reported with wheezing and air-trapping [57]. The lung imaging is characterized by geographic ground-glass opacifications mainly in the right middle lobe and the lingula. On lung biopsy, the abnormal histological findings are minor: hyperplasia of neuroendocrine cells within terminal bronchioles documented by bombesin immunohistochemistry; light thickening of the airway smooth muscle; aspecific increase of the alveolar macrophages [58,59].
Imaging of pancreatic neuroendocrine tumors: recent advances, current status, and controversies
Published in Expert Review of Anticancer Therapy, 2018
Lingaku Lee, Tetsuhide Ito, Robert T. Jensen
In general, all of this has changed. It is now clear that panNETs as well as NETs in other locations are increasing in frequency, and whether it is because of increased detection or increased occurrence is not clear [293]. Also, there have been large strides in the pathology of NETs, with the development of classification/grading systems that have prognostic value and can influence patient management [1,2]. Insights from these pathologic studies have begun to have an impact on therapeutic approaches in other more frequent, aggressive tumors such as prostate cancer [294–296]. From the pathological studies of panNETs and other NETs, it has become clear that they frequently over-express G-protein-coupled receptors from a number of families (especially somatostatin, GLP1, bombesin) and from that arose the concept that these could be used to localize these tumors, as well as later, to treat them [99]. From these observations developed the use of radiolabeled somatostatin analogs to imagine the tumors, which is now the most sensitive localization method available [20,99]. Furthermore, using other radiolabeled somatostatin analogs, it has been possible to treat these tumors, because almost all overexpress somatostatin receptors, if well differentiated [96,99]. This latter point has been shown in a recent Phase-3 study [97]. This methodology is now being investigated for the diagnosis, imaging and treatment of prostate cancer using radiolabeled bombesin receptor analogs [294,295]. Furthermore, it is now realized that a significant proportion of panNETs and NETs in other locations pursue an aggressive course, and can cause considerable morbidity [1–3]. This has led to a number of double-blind Phase-3 studies of antitumor treatment for malignant panNETs and/or patients with other NETs in other locations with advanced diseases [297–300]. These include studies demonstrating the antiproliferative efficacy of somatostatin analogs; the mTOR inhibitor, everolimus and the tyrosine kinase inhibitor, sunitinib [297–300].