Among Patients with Endometriosis, Does the Use of Serum Biomarkers, Versus Laparoscopic Surgery For Diagnosis and Staging of the Disease Decrease the Incidence of Disease Related Negative Outcomes

Objective: To determine the ability and efficacy of non-invasive serum biomarker testing as a replacement for laparoscopic surgery in the diagnosis and staging of endometriosis to decrease the incidence of negative disease outcomes, leading to improvement in the accuracy of diagnoses and patient tailored treatment protocols. Background: Endometriosis is a debilitating inflammatory disease of the reproductive tract. Currently, the gold standard for the diagnosis and staging of endometriosis is exploratory laparoscopic surgery. The use of surgery as the source of achieving a definitive diagnosis holds the potential to increase the incidence of negative disease outcomes. Because of this, the use of peripheral serum biomarkers for the initial diagnosis of endometriosis is being explored as a non- invasive diagnostic option to decrease the incidence of negative disease outcomes. Methods: Articles used were retrieved from PubMed, Google Scholar, Cochrane, Science Direct and UpToDate. Additionally, two individuals who had been surgically diagnosed with endometriosis were interviewed via email. Conclusion: The potential of serum biomarkers as an alternative to laparoscopy to diagnose and stage endometriosis in order to decrease the incidence of negative disease outcomes cannot be ignored. When weighed against the potential risks of surgery, as well as the high incidence of disease recurrence after conservative ablative procedures, peripheral serum biomarkers should be considered the forefront of endometriosis research in order to improve patient outcomes. To achieve this, the scientific community must work in close collaboration with each other, as well as become proficient in the clinical findings of endometriosis in order to achieve adequate and tailored patient centered care

Neuropeptide Y (18–36) modulates chromaffin cell catecholamine secretion by blocking the nicotinic receptor ion

or Poiuu.cowcy AND ExP iuME rr.u. THERAPEuTIC

UTP and ATP increase extracellular signal-regulated kinase 1/2 phosphorylation in bovine chromaffin cells through epidermal growth factor receptor transactivation

Adenosine triphosphate (ATP) is coreleased with catecholamines from adrenal medullary chromaffin cells in response to sympathetic nervous system stimulation and may regulate these cells in an autocrine or paracrine manner. Increases in extracellular signal-regulated kinase (ERK) 1/2 phosphorylation were observed in response to ATP stimulation of bovine chromaffin cells. The signaling pathway involved in ATP-mediated ERK1/2 phosphorylation was investigated via Western blot analysis. ATP and uridine 5′-triphosphate (UTP) increased ERK1/2 phosphorylation potently, peaking between 5 and 15 min. The mitogen-activated protein kinase (MAPK/ERK)-activating kinase (MEK) inhibitor PD98059 blocked this response. UTP, which is selective for G-protein-coupled P2Y receptors, was the most potent agonist among several nucleotides tested. Adenosine 5′-O-(3-thio) triphosphate (ATPγS) and ATP were also potent agonists, characteristic of the P2Y2 or P2Y4 receptor subtypes, whereas agonists selective for P2X receptors or other P2Y receptor subtypes were weakly effective. The receptor involved was further characterized by the nonspecific P2 antagonists suramin and reactive blue 2, which each partially inhibited ATP-mediated ERK1/2 phosphorylation. Inhibitors of protein kinase C (PKC), protein kinase A (PKA), Ca2+/calmodulin-dependent protein kinase II (CaMKII), and phosphoinositide-3 kinase (PI3K) had no effect on ATP-mediated ERK1/2 phosphorylation. The Src inhibitor PP2, epidermal growth factor receptor (EGFR) inhibitor AG1478, and metalloproteinase inhibitor GM6001 decreased ATP-mediated ERK1/2 phosphorylation. These results suggest nucleotide-mediated ERK1/2 phosphorylation is mediated by a P2Y2 or P2Y4 receptor, which stimulates metalloproteinase-dependent transactivation of the EGFR

Effects of α-Phenyl-N-tert-Butyl Nitrone (PBN) on Brain Cell Membrane Function and Energy Metabolism during Transient Global Cerebral Hypoxia-Ischemia and Reoxygenation-Reperfusion in Newborn Piglets

We sought to know whether a free radical spin trap agent, α-phenyl-N-tert-butyl nitrone (PBN) influences brain cell membrane function and energy metabolism during and after transient global hypoxia-ischemia (HI) in the newborn piglets. Cerebral HI was induced by temporary complete occlusion of bilateral common carotid arteries and simultaneous breathing with 8% oxygen for 30 min, followed by release of carotid occlusion and normoxic ventilation for 1 hr (reoxygenation-reperfusion, RR). PBN (100 mg/kg) or vehicle was administered intravenously just before the induction of HI or RR. Brain cortex was harvested for the biochemical analyses at the end of HI or RR. The level of conjugated dienes significantly increased and the activity of Na+, K+-ATPase significantly decreased during HI, and they did not recover during RR. The levels of ATP and phosphocreatine (PCr) significantly decreased during HI, and recovered during RR. PBN significantly decreased the level of conjugated dienes both during HI and RR, but did not influence the activity of Na+, K+-ATPase and the levels of ATP and PCr. We demonstrated that PBN effectively reduced brain cell membrane lipid peroxidation, but did not reverse ongoing brain cell membrane dysfunction nor did restore brain cellular energy depletion, in our piglet model of global hypoxic-ischemic brain injury

Characterization of neuropeptide Y (NPY) receptors in human hippocampus

We identified a 50 kDa neuropeptide Y (NPY) receptor from human hippocampus by affinity labeling. NPY specific binding and labeling of the receptor were inhibited in parallel by increasing concentrations of unlabeled NPY (IC= 0.27nM and0.18nM, respectively). Peptide YY (PYY), but none of the pancreatic polypeptides, was as effective as NPY in displacing [ 125I]NPY. NPY fragments inhibited binding with the rank order of potency: NPY>NPY 13–36 >NPY 20–36≥NPY 18–36 >NPY 1–36free acid≥NPY 26–36. These results demonstrate that the human hippocampal NPY receptor is a 50 kDa protein fitting the classification of a Y 2 receptor subtype

Identifying Important Microphysical Properties and Processes for Marine Fog Forecasts

In this study, a marine fog event that occurred from 0000 to 1800 UTC 7 September 2018 near Canada’s Grand Banks is used to investigate the sensitivity of simulated fog properties to six model parameters found primarily in the microphysics scheme. To do so, we ran a large suite of regional simulations that spanned the life cycle of the fog event using the Regional Atmospheric Modeling System (RAMS). We randomly selected parameter combinations for the simulation suite and used Gaussian process regression to emulate the response of a variety of simulated fog properties to the parameters. We find that the microphysics shape parameter, which controls the relative width of the droplet size distribution, and the aerosol number concentration have the greatest impact on fog in terms of spatial extent, duration, and surface visibility. In general, parameters that reduce mean fall speed of droplets and/or suppress drizzle formation lead to reduced visibility in fog but also delayed onset, shorter lifetimes, and reduced spatial extent. The importance of the distribution width suggests a need for better characterization of this property for fog droplet distributions and better treatment of this property in microphysics schemes

Cysteamine selectively enhances neuropeptide Y2 receptor binding activity

Affinity labeling of [125I]NPY to the bovine hippocampal NPY receptor has revealed a 50 kDa specific binding protein, the Y2 receptor. Cysteamine (10 μM – 10 mM) specifically enhanced NPY specific labeling of the Y2 receptor without affecting crosslinking effeiciency. Several structurally related agents, including reduced glutathione, cysteine, β-mercaptoethanol and ethanolamine, were without effect on receptor binding. The enhancement of binding by cysteamine could be reversed by washing the membranes. These studies suggest that cysteamine may change the conformation of the NPY Y2 receptor and increase its binding activity

A study of climate risk in the Norwegian financial sector

Climate change and the transition to the low-emission society constitute a financial risk that should be included in risk assessments. It is no longer enough to merely report on how the business affects the environment. Climate risk is about how climate change and associated societal changes will constitute a risk for the financial stability. The British Governor, Mark Carney, is even warning that the climate risk may be the starting point of a new financial crisis. The purpose of this study is to analyse whether Norwegian finance companies have started to integrate climate risk considerations. The data basis is in-depth interviews with representatives from six central financial institutions and a qualitative content analysis of their respective annual reports. Furthermore, we have done a quantitative content analysis of annual reports from 15 banks and mortgage companies from 2017 and 2018. The report is based on theory and literature about CSR, the role of banks in the economy and climate risk. The quantitative analysis concludes that climate change can be categorized as the new word of the year in the reporting for 2018. The term went from being mentioned in three of fifteen annual reports in 2017, to ten in 2018. The qualitative analysis shows that four out of six companies state that they plan to report after the Task Force on Climate-related Financial Disclosures (TCFD) recommendations in a longer term. Another important finding is that climate change often is considered as CSR rather than a financial risk. This is, among other things, evident when looking at where the responsibility for climate risk is placed within the organization. Furthermore, we have seen that some of the greatest challenges managing climate risk are the lack of data, methods and knowledge. Banks and mortgage companies in Norway have done little in their work with climate risk, and the danger of a climate-related financial crisis is likely to be present. We therefore recommend that regulatory authorities invest resources to develop tools for managing climate risk. The general lack of competence should be met by entering climate risk into educational plans in the finance education. Furthermore, we encourage industry organizations to facilitate more cooperation to raise the competence in the businesses. Finally, we recommend financial institutions to address the challenges of climate risk for example by giving risk analysts the task of developing methods to meet climate risk.Klimaendringer og overgangen til lavutslippssamfunnet utgjør en finansiell risiko som bør innarbeides i risikovurderinger. Det er ikke lenger nok å bare rapportere om hvordan virksomheten påvirker miljøet. Klimarisiko handler om hvordan klima-endringer kan påvirke finansiell stabilitet. Den britiske sentralbanksjefen, Mark Carney, går så langt som å advare mot at klimaendringer og endringene som følger med kan være utgangspunktet for en ny finanskrise. Formålet med denne studien er å kartlegge hvor langt finansforetak i Norge har kommet i arbeidet med klimarisiko. Datagrunnlaget er dybdeintervjuer med representanter fra seks sentrale finansforetak og en kvalitativ innholdsanalyse av deres respektive årsrapporter. Videre er det gjennomført en kvantitativ innholds-analyse av årsrapporter fra 15 banker og kredittforetak fra 2017 og 2018. Teori og litteratur som danner grunnlaget for rapporten består av bedriftens samfunnsansvar, bankers rolle i økonomien og klimarisiko. Resultatene viser at klimarisiko kan kategoriseres som årets nyord i rapporteringen i 2018. Begrepet gikk fra å være nevnt i tre av femten årsrapporter i 2017, til ti i 2018. Den kvalitative analysen viser at fire av seks foretak oppgir at de planlegger å rapportere etter Task Force on Climate-related Financial Disclosure (TCFD)-anbefalingene på sikt. Et annet viktig funn er at klimaendringer ofte blir betraktet som samfunnsansvar fremfor en finansiell risiko. Dette kommer blant annet til syne gjennom hvor ansvaret for klimarisiko er plassert i organisasjonen. Videre har vi sett at noen av de største utfordringene i arbeidet med klimarisiko er mangel på data, metoder og kunnskap. Bankene og kredittforetak i Norge har gjort lite i arbeidet med klimarisiko, og faren for en klimarelatert finanskrise må kunne antas å være til stede. Vi anbefaler dermed at regulerende myndigheter setter inn ressurser for å utvikle verktøy for å håndtere klimarisiko. Den generelle mangelen på kompetanse bør møtes med å legge inn klimarisiko i utdanningsplaner i økonomiutdanningen. Videre oppfordrer vi bransjeorganisasjoner som Finans Norge å legge til rette for flere samarbeid med mål om å heve kompetansen i virksomhetene. Avslutningsvis anbefaler vi finansforetak å ta tak i utfordringene med klimarisiko, blant annet ved å gi risikoanalytikere i oppgave å utvikle metoder for å møte klimarisiko.  M-Ø