TermPicks: a century of Greenland glacier terminus data for use in scientific and machine learning applications

Marine-terminating outlet glacier terminus traces, mapped from satellite and aerial imagery, have been used extensively in understanding how outlet glaciers adjust to climate change variability over a range of timescales. Numerous studies have digitized termini manually, but this process is labor intensive, and no consistent approach exists. A lack of coordination leads to duplication of efforts, particularly for Greenland, which is a major scientific research focus. At the same time, machine learning techniques are rapidly making progress in their ability to automate accurate extraction of glacier termini, with promising developments across a number of optical and synthetic aperture radar (SAR) satellite sensors. These techniques rely on high-quality, manually digitized terminus traces to be used as training data for robust automatic traces. Here we present a database of manually digitized terminus traces for machine learning and scientific applications. These data have been collected, cleaned, assigned with appropriate metadata including image scenes, and compiled so they can be easily accessed by scientists. The TermPicks data set includes 39 060 individual terminus traces for 278 glaciers with a mean of 136 ± 190 and median of 93 of traces per glacier. Across all glaciers, 32 567 dates have been digitized, of which 4467 have traces from more than one author, and there is a duplication rate of 17 %. We find a median error of ∼ 100 m among manually traced termini. Most traces are obtained after 1999, when Landsat 7 was launched. We also provide an overview of an updated version of the Google Earth Engine Digitization Tool (GEEDiT), which has been developed specifically for future manual picking of the Greenland Ice Sheet

The neuropeptide \uf061-MSH has specific receptors on neutrophils and reduces chemotaxis in vitro

The proopiomelanocortin-derived peptide \u3b1-melanocyte stimulating hormone (\u3b1-MSH) has potent anti-inflammatory effects in all animal models of inflammation against which it has been tested. Understanding of the mechanism by which this occurs is incomplete, although there is recent evidence for \u3b1-MSH receptors in murine and human macrophages and for modulation of production of proinflammatory cytokines and related mediators by \u3b1-MSH. Because of the prominence of neutrophils in early stages of inflammatory reactions where \u3b1-MSH is effective, we examined human neutrophils for evidence of mRNA for \u3b1-MSH receptors and for inhibition of neutrophil chemotaxis. There was accumulation of mRNA for melanocortin receptor 1 (MC1) in RT/PCR product from neutrophils stimulated with interferon and LPS. In subsequent studies \u3b1-MSH inhibited migration of neutrophils from most normal volunteers when the cells were placed in FMLP or IL-8 gradients. The inhibition by \u3b1-MSH could be traced to alterations in cAMP in neutrophils. The presence of \u3b1-MSH receptor message in neutrophils is consistent with the established anti-inflammatory effects of the peptide. Direct inhibition of neutrophil chemotaxis likely contributes to the anti-inflammatory activity of \u3b1-MSH

Anti-inflammatory effects of alpha-melanocyte-stimulating hormone in celiac intestinal mucosa

Objectives: The peptide \u3b1-melanocyte-stimulating hormone (\u3b1-MSH) possesses potent anti-inflammatory activities and has been previously implicated in the endogenous control of inflammatory reactions. The aim of the present research was to determine whether \u3b1-MSH and its receptors participate in a localized anti-inflammatory response in the duodenal mucosa of celiac patients. Methods: Three series of experiments were performed, using duodenal biopsy pairs from 53 adult celiac patients and 14 normal subjects, in order to determine: (1) mucosal immunoreactivity for \u3b1-MSH and melanocortin receptors (MCRs), and gene expression of \u3b1-MSH precursor pro-opiomelanocortin and MCRs; (2) \u3b1-MSH and inflammatory cytokine production by duodenal specimens in vitro, and the influence of synthetic \u3b1-MSH on such cytokine production, and (3) the influence of stimulation with gliadin (the subfraction of gluten that is toxic to patients with celiac disease) on \u3b1-MSH and cytokine production in vitro and the effect of \u3b1-MSH on gliadin-stimulated cytokine production. Results: Elements of a localized anti-inflammatory influence based on \u3b1-MSH and its receptors were found: duodenal mucosa showed immunostaining for \u3b1-MSH and two of its receptor subtypes, MC1R and MC5R. \u3b1-MSH and MC1R immunoreactivity was more intense in specimens from celiac patients. Release of interleukin 6 from gliadin-stimulated duodenal mucosa was inhibited by synthetic \u3b1-MSH in vitro. Conclusions: Presence of \u3b1-MSH and its receptors in celiac mucosa suggests the presence of a local reaction to control the inflammatory response elicited by gliadin. In selected cases of refractory celiac disease, treatment with exogenous peptides might be considered. Copyrigh

Alpha-melanocyte-stimulating hormone is decreased in plasma of patients with acute brain injury

The neuropeptide \u3b1-melanocyte-stimulating hormone (\u3b1-MSH) is a proopiomelanocortin derivative that has potent anti-inflammatory influences within the brain. The aim of the present research was to determine if there are changes in blood concentrations of this peptide in patients with acute traumatic brain injury (TBI) or subarachnoid hemorrhage (SAH). Concomitantly, we recorded clinical parameters and measured blood concentrations of the proinflammatory cytokine tumor necrosis factor-\u3b1 (TNF-\u3b1). Twenty-three patients were enrolled in this study - 18 had TBI and five SAH. Blood samples for determination of \u3b1-MSH and TNF-\u3b1 were collected daily from day 1 to day 4 after injury. Baseline concentration of plasma \u3b1-MSH in patients with acute brain injury of either traumatic or vascular origin was significantly lower than in controls. Patients with TBI or SAH had similar \u3b1-MSH concentrations and the peptide remained consistently low over four post-injury days. Circulating TNF-\u3b1 on day one was measurable in all patients and there was a negative correlation between plasma TNF-\u3b1 and \u3b1-MSH. \u3b1-MSH was measured again after the acute phase in eight patients. The peptide was substantially increased in all subjects except for two who had an unfavorable outcome. From the well-known protective anti-inflammatory influences of \u3b1-MSH in the host, reduction in this circulating peptide may have detrimental consequences in brain injury. The data raise the possibility that restoration of normal circulating \u3b1-MSH through administration of the peptide could be beneficial in patients with brain injury

The neuropeptide alpha-MSH in host defense

The presence of the ancient peptide alpha-melanocyte-stimulating hormone (alpha-MSH) in barrier organs such as gut and skin suggests that this potent anti-inflammatory molecule may be a component of the innate host defense. In tests of antimicrobial activities, alpha-MSH and its fragment KPV showed inhibitory influences against the gram-positive bacterium Staphylococcus aureus and the yeast Candida albicans. Anti-tumor necrosis factor and antimicrobial effects of alpha-MSH suggest that the peptide might likewise reduce replication of human immunodeficiency virus (HIV). Treatment with alpha-MSH reduced HIV replication in chronically and acutely infected human monocytes. At the molecular level, alpha-MSH inhibited activation of the transcription factor NF-kappa B known to enhance HIV expression. alpha-MSH that combines antipyretic, anti-inflammatory, and antimicrobial effects could be useful in the treatment of disorders in which infection and inflammation coexist

Reduced expression of the melanocortin-1 receptor in human liver during brain death

Objective: There is evidence that brain death has detrimental effects on peripheral organs. Clinical and experimental studies on organ donors showed marked inflammation in tissue samples of livers and kidneys collected during brain death. The inflammatory reaction is characterized by release of cytokines and inflammatory cell infiltration. Because melanocortins and their receptors are significant modulators of inflammation, we hypothesized that downregulation of melanocortin receptors during brain death could contribute to enhance inflammation. Methods: Using real-time polymerase chain reaction (PCR) analysis, we determined expression of melanocortin receptors in liver biopsies obtained from brain-dead organ donors before cold ischemia and in normal liver tissue during resection of benign focal lesions of the liver. Tissue biopsies were also ana lyzed for expression of intercellular adhesion molecule-1 (ICAM-1), which has a central function in inflammatory cell migration. Results: Expression of melanocortin-1 receptor (MC1R) mRNA was markedly reduced in liver samples obtained from brain-dead organ donors compared to hepatic tissue collected during resection of benign focal lesions of the liver. Conversely, expression of the adhesion molecule ICAM-1 was significantly increased in livers of brain-dead organ donors. Conclusions: Disruption of the endogenous anti-inflammatory circuit based on MC1R could contribute to tissue damage during brain death

Inhibitory effects of the peptide (CKPV)2 on endotoxin-induced host reactions

Background. \u3b1-Melanocyte stimulating hormone (\u3b1-MSH) is an endogenous peptide that has remarkable anti-inflammatory and antimicrobial effects. These activities have been traced to the C-terminal tripeptide Lys-Pro-Val (KPV). A dimer composed of two KPV sequences connected with a Cys-Cys linker, (CKPV)2, is currently under clinical investigation for antimicrobial use. The present research was designed to evaluate effects of (CKPV)2 on endotoxin-induced host reactions in vitro and in vivo. Materials and methods. Effects of (CKPV)2, KPV, and [Nle4-dPhe7]-\u3b1-MSH (NDP-\u3b1-MSH) on tumor necrosis factor \u3b1 (TNF-\u3b1) production were determined: 1) in human peripheral blood mononuclear cells (PBMC) stimulated with lipopolysaccharide (LPS) in vitro, and 2) in rats injected with LPS i.v. and sacrificed at 1 h. In additional experiments, dialysis peritonitis was induced in rats by adding LPS to dialysis fluid. Net ultrafiltrate was calculated and concentrations of nitrite (NO 2-) and TNF-\u3b1 were measured in blood and peritoneal fluid at 7 h. Results. (CKPV)2 inhibited TNF-\u3b1 production by LPS-stimulated human PBMC. This small peptide was as effective as NDP-\u3b1-MSH and more potent than KPV. Similar effectiveness was observed in vivo: 1 h after LPS injection, the large increase in circulating TNF-\u3b1 was markedly reduced by (CKPV)2 treatment. In LPS-induced peritonitis, (CKPV)2 restored net ultrafiltrate to control values and significantly inhibited concentrations of TNF-\u3b1 and NO2 - both in plasma and in dialysate. Conclusions. The remarkable capacity of (CKPV)2 to inhibit endotoxin-induced host reactions suggests that it may be useful in treatment of inflammatory disorders

Alpha-melanocyte-stimulating hormone peptides inhibit HIV-1 expression in chronically infected promonocytic U1 cells and in acutely infected monocytes

The purpose of the present research was to determine if alpha-melanocyte-stimulating hormone (alpha-MSH) and its C-terminal tripeptide [alpha-MSH (11-13), KPV] alter HIV expression in infected cells. The results indicate that chronically HIV-1-infected promonocytic U1 cells produce alpha-MSH and that immunoneutralization of the endogenous peptide enhances HIV expression. Because U1 cells express the alpha-MSH receptor 1 (MC1R), an autocrine-inhibitory circuit based on the peptide and its receptor likely occurs in these cells. To determine effects of pharmacological concentrations of alpha-MSH peptides on HIV expression, we measured p24 antigen release by TNF-alpha-stimulated U1 cells exposed to a wide range of concentrations of synthetic alpha-MSH and KPV. Viral expression was reduced by both peptides. KPV also effectively reduced HIV replication in acutely infected monocyte-derived macrophages (MDM). The basis of the peptide influence on viral replication is at the transcriptional level; KPV inhibited activation of NF-kappaB that is known to enhance viral expression. Endogenous alpha-MSH likely contributes to natural defense against HIV. However, greater concentrations of synthetic peptide are much more effective in reducing HIV expression in infected cells