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Microanatomy and Chemical Coding of Peptide-Containing Neurons in the Digestive Tract
Published in Edwin E. Daniel, Neuropeptide Function in the Gastrointestinal Tract, 2019
E. Ekblad, R. Håkanson, F. Sundler
GRP, a 27-amino-acid peptide first isolated from the porcine nonantral gastric mucosa,143 is thought to be the mammalian counterpart of bombesin, a 14-amino-acid peptide originally isolated from amphibian skin.144 The C-terminal 7-amino-acid sequence of GRP is identical with that of bombesin. This region is the biologically active portion, are consequently bombesin and GRP have similar biological activity. Other bombesin-like peptides and neuromedin B and neuromedin C, both of which have been isolated from porcine spinal cord.145,146 The human GRP and neuromedin B precursors have been identified.147,148 The GRP precursor consists of 148 amino acids; the signal sequence is followed by GRP and a C-terminal extension peptide. The neuromedin B precursor is 74 amino acids long and contains neuromedin B (NMB-32) next to the signal peptide followed by an extension peptide. Alternative processing of the single GRP precursor RNA transcript may give rise to three different GRP precursors.147 The precursors differ in the C-terminal extension peptide; the structure of GRP itself is unaffected. Two potential cleavage sites within human GRP could generate GRP14—27 (GRP-14), or GRP18—27 (GRP-10). GRP-10 is identical with neuromedin C.
The Genetic Alibi
Published in Roy J. Shephard, Obesity: A Kinesiologist’s Perspective, 2018
The RGS7 gene is located near to the region associated with G-protein 7 signalling [1]. Three other loci with significant linkages to central fat accumulation are close to genes regulating the level of sex steroids [34]. Of four loci associated with susceptibility to hunger [7], the most significant association is with a locus on chromosome 15q24–q25, in the region of the neuromedin-b gene; a mis-sense mutation within this gene strongly increases the desire to eat, with resultant obesity.
Antimicrobial peptides: a promising strategy for lung cancer drug discovery?
Published in Expert Opinion on Drug Discovery, 2020
Farshid Zandsalimi, Sam Talaei, Mehdi Noormohammad Ahari, Shahin Aghamiri, Pourya Raee, Soheil Roshanzamiri, Fatemeh Yarian, Mojgan Bandehpour, Zeinab Zohrab Zadeh
A549 cell line, established via an explant culture of cancerous lung tissue of a 58-year-old Caucasian male patient, is one of the most typically used cell lines for the development of lung cancer therapeutic agents. Additionally, KRAS, KEAP1, KMT2 C, and FAT4 genes are mutated in A549 cells. These cells can be used as an alveolar type II pulmonary epithelial cell model in studies investigating the pharmacodynamics and pharmacokinetics of therapeutic agents. A549 cells can also be inoculated in mice to create cell line derived xenograft mouse models [55–57]. NCI-H1229 is another commonly used NSCLC cell line that is derived from cells originating lymph node. These cells cannot express the tumor suppressor p53 protein as they carry TP53 mutations (homozygous partial deletion). Furthermore, these cells can release the peptide hormone neuromedin B (NMB) [58]. EGFR-TKIs are extensively used for the treatment NSCLCs, which carry EGFR-activating mutations. However, after a month NSCLC cells inevitably obtain resistance to these drugs [59]. PC-9 cells have a mutation in the EGFR gene. As a result, these cells can be a good model for studies in which new strategies for overcoming EGFR-TKIs are investigated [60]. The NCI-H460 cell line was first developed by Gazdar and his colleagues through the culture of pleural fluid of a male patient with large cell lung cancer (a main subtype of NSCLC). These cells have high p53 mRNA expression at levels comparable to normal lung cells. It is noteworthy that DNA structure of these cells is normal [61].
Pharmacotherapy for erectile dysfunction in diabetic males
Published in Expert Opinion on Pharmacotherapy, 2018
A recent study investigated the effect of Neuromedin B on erectile function in a diabetic rat model. The positive effect was associated with conservation of the cavernous body structure and nNOS-expressing nerves, together with recovery of α-smooth muscle actin, vascular endothelial-cadherin, and nNOS expression. Furthermore, neuromedin B significantly stimulated the survival of SH-SY5Y cells derived from human neuroblastoma tissue with characteristics similar to neurons. Collectively, these results suggested that neuromedin B restored erectile function via protection of the cavernous body from injury and stimulated the survival of the associated nerves. Neuromedin B may be useful to treat ED patients with a severely damaged cavernous body [94].
Intranasal trigeminal function in chronic rhinosinusitis: a review
Published in Expert Review of Clinical Immunology, 2023
Anna Kristina Hernandez, Thomas Hummel
Only one study in our review directly investigated the relationship of inflammation with trigeminal function. Zhang et al. found that tissue eosinophil count was correlated with tERP N1 and P2 peak latencies, but not amplitudes, for ethyl alcohol as a stimulus [24]. Also, in the same study, they found a correlation between tERP latency and sneezing visual analogue scale (VAS) ratings, where worse ratings corresponded to longer latencies (Kendall’s tau-b=−0.40, p = 0.005). However, since Kendall’s tau was the analysis used, the quantitative effect this corresponds to is uncertain, as this analysis only gives an ordinal association between the two variables. Sneezing was found to be mediated by TRPV1 in mice [65]. TRPV1+ nasal neurons were found to selectively express neuromedin B, a peptide that activates neuromedin B receptor + (NMBR+) neurons in the area of the brainstem related to sneezing. These NMBR+ neurons were found to synapse with the caudal ventral respiratory group to induce sneezing when prompted by chemical irritants or allergens [65]. Interestingly, however, trigeminal function appears to be preserved, or even better, in allergic rhinitis (AR) patients [23,25,66]. Trigeminal CO2 thresholds (t63 = 2.69; p < 0.05) were lower. Responses to a nasal mucosal signal (negative mucosal potential, NMP) had shorter latencies (N1: t57 = 2.20, p < 0.05; P2: t57 = 2.30, p < 0.05) and tERP P1 (t26 = 2.12, p < 0.05), N1 (t26 = 2.12, p < 0.05), and P2 (t26 = 2.08, p < 0.05) peak latencies were also significantly shorter in patients with AR [25]. Trigeminal lateralization was also found to be significantly better in patients with AR compared to CRS (p = 0.002), but the difference between scores of AR patients and healthy controls remained non-significant [23]. On the other hand, patients with asthma were found to have lower pre-operative scores on chemosensory function tests than patients without asthma (p < 0.005), but having asthma did not influence the effect of surgery on post-operative chemosensory function [19].