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Metallopharmaceuticals
Published in Varma H. Rambaran, Nalini K. Singh, Alternative Medicines for Diabetes Management, 2023
Varma H. Rambaran, Nalini K. Singh
Finally, an investigation by Liu et al. demonstrated the influence of molybdate treatment on the increase in cellular-insulin content and the enhancement of basal insulin release, by clonal BRIN BD11 cells. Further to this, the team reported a desirable improvement in the responsiveness to glucose and a wide range of other secretagogues (Liu et al. 2004).
Mast Cell Activation and Leukocyte Recruitment Responses Into Skin Sites
Published in Bruce S. Bochner, Adhesion Molecules in Allergic Disease, 2020
Michael D. Ioffreda, George F. Murphy
Secretagogues are substances that cause mast cells to release their mediators by a process termed degranulation, whereby membrane-bound cytoplasmic granules undergo rapid exocytosis (Fig. 1A-D). Mast cell secretagogues include the neuropeptide substance P, morphine sulfate, compound 48/80, calcium ionophore, the complement components C3a and C5a, major basic protein, and histaminereleasing factors (HRF), including macrophage inflammatory protein-1α (MIP-1α) and monocyte chemoattractant peptide-1 (MCP-1) (16,19,20). Mast cell mediator release can also be initiated by proteins or factors that cross-link IgE bound to high-affinity Fce receptors on the mast cell surface (21,22). The IgE response is characteristic of mast cell degranulation in type I reactions and is prototypical of the ability of many secretagogues to induce granule discharge within minutes of exposure (“anaphylactic degranulation”). In addition, unmyelinated type C sensory nerve fibers originating in the dorsal root ganglion release neurotransmitters that impact on tissue mast cells as a result of retrograde impulses (reviewed in ref. 20). The neuropeptides substance P, vasoactive intestinal peptide (VIP), neurokinin A and B, somatostatin, calcitonin gene related peptide, and adenosine nucleotides have been recognized as mast cell degranulating agents
Psychological Effects of Exercise for Disease Resistance and Health Promotion
Published in Ronald R. Watson, Marianne Eisinger, Exercise and Disease, 2020
While the hypothalamus mediates HPA feedback, it appears subordinate to higher command. For example, deafferentation of the hypothalamus leads to resistance to dexamethasone suppression of ACTH. Sopolsky60 argues that the hippocampus exerts an inhibitory central command on the hypothalamus and that damage or disruption of hippocampal activity can explain part of the hypercortisolism of depression. He has shown that sustained exposure to stressors also is associated with decreased receptor density in hippocampus. In addition to CRF, AVP, OT, catecholamines, and angiotensin stimulate ACTH directly or in synergy with CRF. The pattern of secretagogues appears stereotyped for different stressors.53 Thus, it will be important to determine if exercise and depression share common patterns while examining the plausibility that either acute or chronic exercise might influence HPA regulation by influencing hippocampal activity or regulation.
Efficacy and safety of iguratimod on patients with primary Sjögren’s syndrome: a randomized, placebo-controlled clinical trial
Published in Scandinavian Journal of Rheumatology, 2021
Q Shao, S Wang, H Jiang, L Liu
The primary endpoint was the EULAR Sjögren’s Syndrome Patient Reported Index (ESSPRI) score at week 24. The secondary endpoints were mental discomfort visual analogue scale (VAS) score, patient global assessment (PGA) (normal–severe, 0–10), EULAR Sjögren’s Syndrome Disease Activity Index (ESSDAI) score, Schirmer’s test values, and salivary flow values. Schirmer’s test was carried out by placing a tear test filter paper in the lower fornix of the conjunctiva of the eye. The length of wetting was measured after 5 min. Salivary flow was measured using the whole saliva technique. Participants were instructed to withhold their dose of any secretagogue (pilocarpine or cevimeline) for 48 h before the visit and to take nothing by mouth for 60 min or longer before saliva collection. The unstimulated whole salivary flow (UWSF) was measured for 15 min. Each follow-up examination was undertaken in the outpatient department, at weeks 4, 8, 12, 18, and 24 ± 3 days.
Harpagoside-induced anaphylactic reaction in an IgE-independent manner both in vitro and in vivo
Published in Immunopharmacology and Immunotoxicology, 2018
Delu Che, Jiao Cao, Rui Liu, Jue Wang, Yajing Hou, Tao Zhang, Nan Wang
Mast cells are classically considered to trigger allergic and anaphylactic reactions. The most widely studied mechanism by which mast cells become activated is the cross-linking of FcεRI, with mast cells responding to antigenic stimulation through the cross-linking of immunoglobulin E (IgE) bound to high-affinity receptors for IgE (FcεRI), and activation of FcγR after IgG binding6. Once activated, intracellular Ca2+ influx increases rapidly and triggers the release of mediators including histamine, β-hexosaminidase, proteases (mainly tryptase), mast cell carboxypeptidase A3 and chymase, platelet-activating factor and prostaglandins7. These substances induce allergic responses, local swelling and asthma, which are common symptoms of allergy. A unique characteristic of mast cells is their antibody-independent responsiveness pathway8,9. This pathway is activated by a variety of basic compounds collectively known as basic secretagogues, which includes peptides and amines such as substance P, mast cell degranulating peptide, neuropeptide Y, mastoparan, and compound 48/8010. In this study, we examined the anaphylactic effects of HAR both in vitro and in vivo.
Tenapanor for the treatment of irritable bowel syndrome with constipation
Published in Expert Review of Clinical Pharmacology, 2020
Emanuele Sinagra, Francesca Rossi, Dario Raimondo, Giuseppe Conoscenti, Andrea Anderloni, Valentina Guarnotta, Marcello Maida
The authors identified 15 eligible-randomized controlled trials of secretagogues that included 8462 patients. In this study, linaclotide, lubiprostone, plecanatide, and tenapanor were superior to placebo for the treatment of IBS-C [44]. While linaclotide (290 μg once daily) was ranked first in efficacy based on the end point recommended by the Food and Drug Administration for trials in IBS-C, the primary end point used in each trial, abdominal pain, and CSBM, tenapanor (50 mg twice daily) was ranked first for decreasing bloating [44].