Utvikling og skader i plantefelt med granplanter fra Lyngdal frøplantasje og handelsprovenienser

Vi registrerte plantenes utvikling og skader og målte høyder på 103 plantefelt med gran i Sør-Trøndelag, Nord-Trøndelag og Nordland, og på åtte kontrollfelt med flere plantepartier. Frøet kom enten fra Lyngdal frøplantasje eller lokale provenienser (bestandsfrø). Formålet var å beskrive effekter av krysningsmiljøet i frøplantasjen (ettereffekter), som er påvist i planteskoler og i forsøk, på utviklingen i plantefelt. Resultatene tyder på at tilstanden i plantefelt med planter fra lyngdalfrø og fra bestandsfrø gjennomsnittlig er noenlunde lik. Det er allikevel variasjon i resultatene både for regioner (kyst- og indre strøk) og for egenskapene som er studert. I kyststrøk er utviklingen omtrent den samme for planter fra de to gruppene, men med et litt høyere plantetall for feltene med bestandsfrø. I midtre og indre strøk er det noe bedre utvikling på feltene med planter fra bestandsfrø enn på de fra bestandsfrø. I Nordland og i høyereliggende strøk i Nord-Trøndelag har planter fra plantasjefrø klart seg like godt som lokal proveniens. Endelige konklusjoner om bruksområder for frø fra Lyngdal frøplantasje bør trekkes etter en total vurdering av alle resultater fra både tidlige tester, avkomforsøk og plantefelt.publishedVersio

Gonadotropin-releasing hormone analog buserelin causes neuronal loss in rat gastrointestinal tract.

Gonadotropin-releasing hormone (GnRH) analogs are given to women undergoing in vitro fertilization. Case reports describing the development of chronic intestinal pseudo-obstruction and auto-antibodies against GnRH after such treatment suggest a strong association between intestinal dysfunction and GnRH analogs. No experimental model for studying such a relationship is currently at hand. Our main goal was to investigate possible enteric neurodegeneration and titers of GnRH antibodies in response to repeated administration of the GnRH analog buserelin in rat. Rats were treated for 1-4 sessions with daily subcutaneous injections of buserelin or saline for 5 days, followed by 3 weeks of recovery. Buserelin treatment caused significant loss of submucous and myenteric neurons in the fundus, ileum, and colon. The loss of enteric neurons can, at least partly, be explained by increased apoptosis. No GnRH- or GnRH-receptor-immunoreactive (IR) enteric neurons but numerous luteinizing hormone (LH)-receptor-IR neurons were detected. After buserelin treatment, the relative number of enteric LH-receptor-IR neurons decreased, whereas that of nitric-oxide-synthase-IR neurons increased. No intestinal inflammation or increased levels of circulating interleukins/cytokines were noted in response to buserelin treatment. Serum GnRH antibody titers were undetectable or extremely low in all rats. Thus, repeated administrations of buserelin induce neurodegeneration in rat gastrointestinal tract, possibly by way of LH-receptor hyperactivation. The present findings suggest that enteric neurodegenerative effects of GnRH analog treatment in man can be mimicked in rat. However, in contrast to man, no production of GnRH auto-antibodies has been noted in rat

The precautionary principle in the EU: Why a formal review is long overdue

This article, through a series of case studies, ranging from European court cases to the Swedish decision to ban Bisphenol A, shows how regulators, policy makers and the European courts are misinterpreting the precautionary principle and not following the European Commission's Communication on the topic. In conclusion, the article puts forward a number of short-term and long-term recommendations on how to make the precautionary principle more evidence based and risk informed going forward. Among the recommendations highlighted include the updating of the Communication on the precautionary principle, establishing a proper European academy of sciences and training regulators and policy makers in evidence-based risk communication.</p