Environmental assessment of certain plans and programmes as contribution to sustainable spatial development

Cities and urban regions especially in the West German agglomerations are characterised by an unbroken dynamic development, connected with changes in land use from undeveloped land into settlement areas and traffic zones up to the rural districts far from the cities. Environmental loads, e.g. negative environmental effects on air quality and noise, and adverse affects on valuable habitats are negative consequences of the growing of urban regions. On the other hand, cities and urban regions shall contribute to a sustainable spatial development as agreed to in the Agenda 21 and prescribed by the Regional Planning Law and the Federal Building Code. In order to turn the spatial development of cities and urban regions towards a sustainable spatial development, adequate planning and management instruments are required. The Directive of the European Union on the assessment of the effects of certain plans and programmes on the environment contains a framework, how the member states will have to take into consideration environmental aspects while drawing up or complementing certain plans and programmes. An environmental assessment shall be carried out for plans and programmes, which are likely to have significant environmental effects, e.g. for town and country planning and land use planning, and which set the framework for future development for projects submitted to an environmental impact assessment. The environmental assessment shall take into consideration reasonable alternatives including the zero-alternative. It shall contain a "screening" (necessity-check), a "scoping" (agreement on the scope of investigations), an "environmental report" and consultations of the public. The environmental report shall contain the analyse and evaluation of likely significant positive and negative effects on biodiversity, population and human health, fauna, flora, soil, water, air, climatic factors, material assets, cultural heritage including architectural and archaeological heritage. The Member States shall bring into force the laws, regulations and administrative provisions necessary to comply the Directive up to 2004. The discussion on the implementation of the EU Directive is in full swing. In Germany, each drawing up of a new land use plan or regional plan will require an environmental assessment. In the case of changes or amendments of those plans, it will depend a.o. on the extent and amount of environmental effects of the plan, whether an environmental assessment has to be carried out or not. Whether and how an environmental assessment can be integrated into spatial planning, and whether the landscape plans already carry out environmental assessments or have to be developed further is under discussion controversially. Further questions are e.g. how the subjects of the assessment shall be defined in detail, how results of the environmental assessment can be monitored, how the environmental assessment can be integrated into the planning procedures without taking many financial and personal resources, and how and at which extent the public shall be consulted. The lecture will focus on how the Directive can be realised by spatial and landscape planning, especially which methodical questions spatial and landscape planning will have to solve in order to implement an environmental assessment for plans and programmes according to the EU Directive.

Environmental assessment of certain plans and programmes as contribution to sustainable spatial development

Cities and urban regions especially in the West German agglomerations are characterised by an unbroken dynamic development, connected with changes in land use from undeveloped land into settlement areas and traffic zones up to the rural districts far from the cities. Environmental loads, e.g. negative environmental effects on air quality and noise, and adverse affects on valuable habitats are negative consequences of the growing of urban regions. On the other hand, cities and urban regions shall contribute to a sustainable spatial development as agreed to in the Agenda 21 and prescribed by the Regional Planning Law and the Federal Building Code. In order to turn the spatial development of cities and urban regions towards a sustainable spatial development, adequate planning and management instruments are required. The Directive of the European Union on the assessment of the effects of certain plans and programmes on the environment contains a framework, how the member states will have to take into consideration environmental aspects while drawing up or complementing certain plans and programmes. An environmental assessment shall be carried out for plans and programmes, which are likely to have significant environmental effects, e.g. for town and country planning and land use planning, and which set the framework for future development for projects submitted to an environmental impact assessment. The environmental assessment shall take into consideration reasonable alternatives including the zero-alternative. It shall contain a "screening" (necessity-check), a "scoping" (agreement on the scope of investigations), an "environmental report" and consultations of the public. The environmental report shall contain the analyse and evaluation of likely significant positive and negative effects on biodiversity, population and human health, fauna, flora, soil, water, air, climatic factors, material assets, cultural heritage including architectural and archaeological heritage. The Member States shall bring into force the laws, regulations and administrative provisions necessary to comply the Directive up to 2004. The discussion on the implementation of the EU Directive is in full swing. In Germany, each drawing up of a new land use plan or regional plan will require an environmental assessment. In the case of changes or amendments of those plans, it will depend a.o. on the extent and amount of environmental effects of the plan, whether an environmental assessment has to be carried out or not. Whether and how an environmental assessment can be integrated into spatial planning, and whether the landscape plans already carry out environmental assessments or have to be developed further is under discussion controversially. Further questions are e.g. how the subjects of the assessment shall be defined in detail, how results of the environmental assessment can be monitored, how the environmental assessment can be integrated into the planning procedures without taking many financial and personal resources, and how and at which extent the public shall be consulted. The lecture will focus on how the Directive can be realised by spatial and landscape planning, especially which methodical questions spatial and landscape planning will have to solve in order to implement an environmental assessment for plans and programmes according to the EU Directive

Untersuchung der Apoptose in kardialen und kardiovaskulären Erkrankungen: Bedeutung von Stickstoffmonoxid

Die Bedeutung der Apoptose und die zugrundeliegenden Mechanismen in verschiedenen pathophysiologischen Zuständen des Herzens sind noch weitgehend ungeklärt und es bleibt zu zeigen, daß die Apoptose-Signaltransduktion ähnlich reguliert wird, wie aus in vitro-Versuchen bekannt ist. Deshalb wurde die Apoptose in verschiedenen Tiermodellen kardialer Erkrankungen untersucht werden, um Hinweise auf die zugrundeliegende Signal-transduktion, durch Analyse der Proteine Bcl-2 und Bax, der finalen Exekutor-Caspase Caspase-3 oder p53 zu bekommen. Apoptose in der durch Hyperlipidämie induzierten Atherosklerose: In Aorten von 'Froxfield Heritable Hypercholesterolemic'-Kaninchen (genetische Hyperlipidämie) korrelierte die Apoptose von vaskulären glatten Muskelzellen und Makrophagen in fortgeschrittenen fibrösen Plaques mit einem 18-fachen Anstieg des proapoptotischen Bax. In Aorten Cholesterin gefütterter 'New Zealand White'-Kaninchen (0,25% Cholest., 12 Wochen) konnte eine erhöhte Baxexpression in Endothelzellen nachgewiesen werden, ohne daß morphologische Veränderungen zu beobachten waren. Die Apoptose in akut abgestoßenen allogenen Herztransplantaten (Rattenmodell) war von einer erhöhten Bax-Expression und einer totalen, posttranslationalen Degradation des antiapoptotischen Bcl-2 in ein spezifisches Degradationsprodukt durch eine Serinprotease gekennzeichnet. Die Rolle des wichtigen kardiovaskulären Mediators Stickstoffmonoxid (NO) auf die Apoptose wird kontrovers diskutiert. Da in der Zellkultur protektive Effekte von NO gezeigt werden konnten, wurde deren physiologische Relevanz in der durch Ischämie/Reperfusion induzierten Apoptose ex vivo im Langendorff-Rattenherzen untersucht. Es konnte gezeigt werden, daß Hemmung der endogenen NO-Synthese mit L-NG-Monomethyl-L-Arginin (LNMMA, 1mM) die Apoptose potenzierte und mit einer Aktivierung der Caspase-3 korrelierte. Bcl-2 und Bax wurden nicht reguliert. Untersuchung der Regulation der Proteinexpression der eNOS (endotheliale NO-Synthase) durch den proinflammatorischen/ proatherogenen Tumor-Nekrose-Faktor-[Alpha] (TNF[Alpha]) in der Endothelzellkultur (HUVEC) gaben Hinweise auf einen, die eNOS schützenden, Interaktionspartner. Zusammenfassend konnte in allen untersuchten Modellen für Herz(-Kreislauf)-Krankheiten Apoptose nachgewiesen werden, die jeweils spezifische Charakteristika zeigt, deren genauere Aufklärung interessante Ziele zukünftiger präventiver und therapeutischer Maßnahmen verspricht. Die Befunde weisen zudem auf antiapoptotische Effekte von NO - insbesondere durch die endotheliale NO-Synthaseaktivität - hin, deren genauere Charakterisierung dazu beitragen könnte, pathophysiologische Zustände der kardiovaskulären Biologie zu erklären.Apoptosis is a distinct form of cell death that has been under intensive investigations in the past few years. Many signalling pathways were elucidated in cell-free systems or in intact cells. But only little is known about apoptosis in cardiac and cardiovascular diseases. Therefore, the aim of this study was to investigate apoptosis in various cardiac diseases: in hyperlipidemia induced atherosclerosis, in acute rejected heart transplants, in ischemia and reperfusion as well as in chronic hypoxia. Atherosclerosis is the main contributor to myocardial infarction. Also hyperlipidemia is a known major risk factor. To investigate apoptosis in hyperlipidemia induced atherosclerosis, genetically induced hyperlipidemia in Froxfield Heritable Hypercholesterolemic Rabbits (FFH, n=8) was compared with New Zealand White rabbits either fed with a cholesterol diet (H, n=8, 0,25% cholesterol, 3% coconut oil) or with a normal diet (control, n=5) for 12 weeks. To determine apoptosis DNA-laddering and immunohistochemical TUNEL-stainings were performed. In advanced fibrous plaques of FFH rabbits apoptosis of vascular smooth muscle cells (VSMCs) and macrophages (M|os) correlated with a drastic 18-fold increased expression of proapoptotic Bax. The antiapoptotic protein Bcl-2 remained unchanged. In conclusion, apoptosis in advanced plaques seems to be a double edged sword: apoptosis of VSMCs may lead to plaque rupture due to diminished collagen synthesis and following myocardial infarction. In contrast, apoptosis of M|o could induce plaque stabilisation. Cholesterol diet did not induce morphological changes of the aortas in spite of elevated serum cholesterol. A doubling of Bax expression was observed in endothelial cells, indicating the induction of apoptosis in this cell type. Apoptosis of endothelial cells could be an initial manifestation leading to endothelial dysfunction and subsequent plaque development. The increased expression of Bax seems to correlate with elevated Low Density Lipoprotein (LDL) levels in both models underlining the induction of apoptosis by elevated serum LDL. Heart transplantation is a common therapeutical option in the terminal stages of heart failure. The most important complications are acute rejection and chronic vasculopathy of the transplants. To investigate apoptosis as an effector mechanism of acute rejection, the model of allogenic heart transplantation from Wistar Furth to Lewis rats (n = 15) was used. These hearts were rejected from 6 to 10 days after transplantation. Apoptosis in acute rejected heart transplants was characterised by an enhanced (3-fold) expression of Bax. Bcl-2 was completely degraded into a specific degradation product of about 17 kD. An RNase protection assay with multiple probes revealed no transcriptional changes of mRNA levels in acute rejected compared to control hearts. The posttranscriptional degradation of Bcl-2 was further analysed in a radioactive assay in vitro. The involvement of a serine protease which is sensitive to nitric oxide (NO) and dithiotreitol (DTT) was eludicated. Apoptosis and in particular the elevated ratio of proapoptotic Bax to antiapoptotic Bcl-2 could be responsible for transplant rejection. In addition, the degradation of Bcl-2 could also contribute to transplant rejection probably due to diminished antiapoptotic Bcl-2 levels or by producing an apoptotic degradation fragment. Myocardial infarction is either a consequence of atherosclerotic vessel occlusion or of transplantation. Typically it is accompanied by a loss of cardiomyocytes. Ischemia/ reperfusion is an accepted model for myocardial infarction. To investigate apoptosis in ischemia/reperfusion, hearts from male Wistar Furth rats were perfused ex vivo in a Langendorff apparatus (n=6 per group; 30 minutes equilibration, 30 min. global ischemia, 30 min. reperfusion). Reperfusion, but not ischemia alone induced apoptosis. Apoptosis was accompanied by the activation of caspase-3, a member of the apoptosis inducing caspase-cascade (as determined by western blotting and a radioactive assay in vitro). In contrast to acute hypoxia in ischemia, chronic hypoxia in Wistar Furth rats (21 days 10% O2, n=4) resulted in apoptosis of the hearts which was characterised by a doubling of proapoptotic Bax and a halffold reduction of antiapoptotic Bcl-2. Thus the enhanced ratio of Bax to Bcl-2 could be responsible for apoptosis in chronic hypoxia. Myocardial diseases are often accompanied by a reduction of endogenous nitric oxide. The role of nitric oxide in apoptosis is discussed controversially. The physiological relevance of antiapoptotic NO-effects was demonstrated in ischemia/ reperfusion experiments. Inhibiting the endogenous NO-synthase in ischemia/reperfusion with its competitive inhibitor L-NG-Monomethyl-L-arginine (LNMMA, 1 mM) potentiated apoptosis. In addition, caspase-3 was activated suggesting protective effects of the endogenous NO production due to an inhibiting interference with caspase-3. These results were underlined by the observations that hearts of endothelial nitric oxide synthase (eNOS)-knockout-mice (n=2 per group) showed apoptosis, which correlated with an elevated Bax expression. All taken together, apoptosis was demonstrated in all models under investigation. Apoptosis shows specific characteristic features in the distinct cardiac/cardiovascular diseases providing future targets for prevention and therapy. Proatherosclerotic and proinflammatoric factors are known to inhibit endogenous NO release. Therefore, the regulation of eNOS protein synthesis in response to tumour necrosis factor [Alpha] (TNF[Alpha]) in the presence of cycloheximide (CHX, an inhibitor of protein synthesis) was analysed in human umbilical vein endothelial cell cultures (HUVEC). The apoptotic stimuli TNF[Alpha]/CHX resulted in the proteolysis of eNOS. The diminished eNOS protein levels were accompanied by a reduced enzyme activity suggesting an antiapoptotic function of the endogenous NO synthesis. Inhibition of the proteasome with ZLLLH, a proteasome-specific inhibitor, only reversed eNOS proteolysis induced by TNF[Alpha]/CHX indicating the involvement of a protein which is interacting with eNOS. eNOS itself seems not to be degraded by the proteasome, because ZLLLH had no effect on TNF[Alpha] induced degradation. In conclusion, these results suggest the presence of a protective eNOS associated protein which is degraded by TNF/CHX leading to a subsequent degradation of eNOS. The chaperone Hsp90 could be such an eNOS interacting protein. However, in our system we could not observe a significant role of HSP70 or Caveolin-1 in eNOS degradation. Immunoprecipitation studies revealed the involvement of an eNOS interacting protein of around 70 kD molecular weight. This protein has still to be identified. In summary, nitric oxide, especially derived from eNOS, seems to be protective against apoptotic cell death. Elucidating the mechanisms leading to a decreased NO production by the eNOS could help to explain pathological disorders of the cardiovascular biology

Environmental Assessment of Certain Plans and Programmes as Contribution to a Sustainable Spatial Development

Abstract A sustainable spatial development requires adequate planning and management instruments; environmental assessments for plans and programmes are considered one of those instruments. Although the concrete way to implement environmental assessments in the German planning system is not yet decided, one can ascertain needs for development of spatial and landscape planning nearly independent from the concrete implementation form

Untersuchung der Apoptose in kardialen und kardiovaskulären Erkrankungen : Bedeutung von Stickstoffmonoxid

Die Bedeutung der Apoptose und die zugrundeliegenden Mechanismen in verschiedenen pathophysiologischen Zuständen des Herzens sind noch weitgehend ungeklärt und es bleibt zu zeigen, daß die Apoptose-Signaltransduktion ähnlich reguliert wird, wie aus in vitro-Versuchen bekannt ist. Deshalb wurde die Apoptose in verschiedenen Tiermodellen kardialer Erkrankungen untersucht werden, um Hinweise auf die zugrundeliegende Signal-transduktion, durch Analyse der Proteine Bcl-2 und Bax, der finalen Exekutor-Caspase Caspase-3 oder p53 zu bekommen. Apoptose in der durch Hyperlipidämie induzierten Atherosklerose: In Aorten von \u27Froxfield Heritable Hypercholesterolemic\u27-Kaninchen (genetische Hyperlipidämie) korrelierte die Apoptose von vaskulären glatten Muskelzellen und Makrophagen in fortgeschrittenen fibrösen Plaques mit einem 18-fachen Anstieg des proapoptotischen Bax. In Aorten Cholesterin gefütterter \u27New Zealand White\u27-Kaninchen (0,25% Cholest., 12 Wochen) konnte eine erhöhte Baxexpression in Endothelzellen nachgewiesen werden, ohne daß morphologische Veränderungen zu beobachten waren. Die Apoptose in akut abgestoßenen allogenen Herztransplantaten (Rattenmodell) war von einer erhöhten Bax-Expression und einer totalen, posttranslationalen Degradation des antiapoptotischen Bcl-2 in ein spezifisches Degradationsprodukt durch eine Serinprotease gekennzeichnet. Die Rolle des wichtigen kardiovaskulären Mediators Stickstoffmonoxid (NO) auf die Apoptose wird kontrovers diskutiert. Da in der Zellkultur protektive Effekte von NO gezeigt werden konnten, wurde deren physiologische Relevanz in der durch Ischämie/Reperfusion induzierten Apoptose ex vivo im Langendorff-Rattenherzen untersucht. Es konnte gezeigt werden, daß Hemmung der endogenen NO-Synthese mit L-NG-Monomethyl-L-Arginin (LNMMA, 1mM) die Apoptose potenzierte und mit einer Aktivierung der Caspase-3 korrelierte. Bcl-2 und Bax wurden nicht reguliert. Untersuchung der Regulation der Proteinexpression der eNOS (endotheliale NO-Synthase) durch den proinflammatorischen/ proatherogenen Tumor-Nekrose-Faktor-[Alpha] (TNF[Alpha]) in der Endothelzellkultur (HUVEC) gaben Hinweise auf einen, die eNOS schützenden, Interaktionspartner. Zusammenfassend konnte in allen untersuchten Modellen für Herz(-Kreislauf)-Krankheiten Apoptose nachgewiesen werden, die jeweils spezifische Charakteristika zeigt, deren genauere Aufklärung interessante Ziele zukünftiger präventiver und therapeutischer Maßnahmen verspricht. Die Befunde weisen zudem auf antiapoptotische Effekte von NO - insbesondere durch die endotheliale NO-Synthaseaktivität - hin, deren genauere Charakterisierung dazu beitragen könnte, pathophysiologische Zustände der kardiovaskulären Biologie zu erklären.Apoptosis is a distinct form of cell death that has been under intensive investigations in the past few years. Many signalling pathways were elucidated in cell-free systems or in intact cells. But only little is known about apoptosis in cardiac and cardiovascular diseases. Therefore, the aim of this study was to investigate apoptosis in various cardiac diseases: in hyperlipidemia induced atherosclerosis, in acute rejected heart transplants, in ischemia and reperfusion as well as in chronic hypoxia. Atherosclerosis is the main contributor to myocardial infarction. Also hyperlipidemia is a known major risk factor. To investigate apoptosis in hyperlipidemia induced atherosclerosis, genetically induced hyperlipidemia in Froxfield Heritable Hypercholesterolemic Rabbits (FFH, n=8) was compared with New Zealand White rabbits either fed with a cholesterol diet (H, n=8, 0,25% cholesterol, 3% coconut oil) or with a normal diet (control, n=5) for 12 weeks. To determine apoptosis DNA-laddering and immunohistochemical TUNEL-stainings were performed. In advanced fibrous plaques of FFH rabbits apoptosis of vascular smooth muscle cells (VSMCs) and macrophages (M|os) correlated with a drastic 18-fold increased expression of proapoptotic Bax. The antiapoptotic protein Bcl-2 remained unchanged. In conclusion, apoptosis in advanced plaques seems to be a double edged sword: apoptosis of VSMCs may lead to plaque rupture due to diminished collagen synthesis and following myocardial infarction. In contrast, apoptosis of M|o could induce plaque stabilisation. Cholesterol diet did not induce morphological changes of the aortas in spite of elevated serum cholesterol. A doubling of Bax expression was observed in endothelial cells, indicating the induction of apoptosis in this cell type. Apoptosis of endothelial cells could be an initial manifestation leading to endothelial dysfunction and subsequent plaque development. The increased expression of Bax seems to correlate with elevated Low Density Lipoprotein (LDL) levels in both models underlining the induction of apoptosis by elevated serum LDL. Heart transplantation is a common therapeutical option in the terminal stages of heart failure. The most important complications are acute rejection and chronic vasculopathy of the transplants. To investigate apoptosis as an effector mechanism of acute rejection, the model of allogenic heart transplantation from Wistar Furth to Lewis rats (n = 15) was used. These hearts were rejected from 6 to 10 days after transplantation. Apoptosis in acute rejected heart transplants was characterised by an enhanced (3-fold) expression of Bax. Bcl-2 was completely degraded into a specific degradation product of about 17 kD. An RNase protection assay with multiple probes revealed no transcriptional changes of mRNA levels in acute rejected compared to control hearts. The posttranscriptional degradation of Bcl-2 was further analysed in a radioactive assay in vitro. The involvement of a serine protease which is sensitive to nitric oxide (NO) and dithiotreitol (DTT) was eludicated. Apoptosis and in particular the elevated ratio of proapoptotic Bax to antiapoptotic Bcl-2 could be responsible for transplant rejection. In addition, the degradation of Bcl-2 could also contribute to transplant rejection probably due to diminished antiapoptotic Bcl-2 levels or by producing an apoptotic degradation fragment. Myocardial infarction is either a consequence of atherosclerotic vessel occlusion or of transplantation. Typically it is accompanied by a loss of cardiomyocytes. Ischemia/ reperfusion is an accepted model for myocardial infarction. To investigate apoptosis in ischemia/reperfusion, hearts from male Wistar Furth rats were perfused ex vivo in a Langendorff apparatus (n=6 per group; 30 minutes equilibration, 30 min. global ischemia, 30 min. reperfusion). Reperfusion, but not ischemia alone induced apoptosis. Apoptosis was accompanied by the activation of caspase-3, a member of the apoptosis inducing caspase-cascade (as determined by western blotting and a radioactive assay in vitro). In contrast to acute hypoxia in ischemia, chronic hypoxia in Wistar Furth rats (21 days 10% O2, n=4) resulted in apoptosis of the hearts which was characterised by a doubling of proapoptotic Bax and a halffold reduction of antiapoptotic Bcl-2. Thus the enhanced ratio of Bax to Bcl-2 could be responsible for apoptosis in chronic hypoxia. Myocardial diseases are often accompanied by a reduction of endogenous nitric oxide. The role of nitric oxide in apoptosis is discussed controversially. The physiological relevance of antiapoptotic NO-effects was demonstrated in ischemia/ reperfusion experiments. Inhibiting the endogenous NO-synthase in ischemia/reperfusion with its competitive inhibitor L-NG-Monomethyl-L-arginine (LNMMA, 1 mM) potentiated apoptosis. In addition, caspase-3 was activated suggesting protective effects of the endogenous NO production due to an inhibiting interference with caspase-3. These results were underlined by the observations that hearts of endothelial nitric oxide synthase (eNOS)-knockout-mice (n=2 per group) showed apoptosis, which correlated with an elevated Bax expression. All taken together, apoptosis was demonstrated in all models under investigation. Apoptosis shows specific characteristic features in the distinct cardiac/cardiovascular diseases providing future targets for prevention and therapy. Proatherosclerotic and proinflammatoric factors are known to inhibit endogenous NO release. Therefore, the regulation of eNOS protein synthesis in response to tumour necrosis factor [Alpha] (TNF[Alpha]) in the presence of cycloheximide (CHX, an inhibitor of protein synthesis) was analysed in human umbilical vein endothelial cell cultures (HUVEC). The apoptotic stimuli TNF[Alpha]/CHX resulted in the proteolysis of eNOS. The diminished eNOS protein levels were accompanied by a reduced enzyme activity suggesting an antiapoptotic function of the endogenous NO synthesis. Inhibition of the proteasome with ZLLLH, a proteasome-specific inhibitor, only reversed eNOS proteolysis induced by TNF[Alpha]/CHX indicating the involvement of a protein which is interacting with eNOS. eNOS itself seems not to be degraded by the proteasome, because ZLLLH had no effect on TNF[Alpha] induced degradation. In conclusion, these results suggest the presence of a protective eNOS associated protein which is degraded by TNF/CHX leading to a subsequent degradation of eNOS. The chaperone Hsp90 could be such an eNOS interacting protein. However, in our system we could not observe a significant role of HSP70 or Caveolin-1 in eNOS degradation. Immunoprecipitation studies revealed the involvement of an eNOS interacting protein of around 70 kD molecular weight. This protein has still to be identified. In summary, nitric oxide, especially derived from eNOS, seems to be protective against apoptotic cell death. Elucidating the mechanisms leading to a decreased NO production by the eNOS could help to explain pathological disorders of the cardiovascular biology

Mentoring for young female practitioners and scientists in spatial and environmental planning in Germany - experiences of the joint mentoring program of the Academy for Spatial Research and Planning and the Association for Spatial and Environmental Research

In order to overcome the underrepresentation of women on higher management levels in planning, the Academy for Spatial Research and Planning (ARL) and the Association for Spatial and Environmental Research (FRU) in Germany jointly have elaborated a mentoring program for young female planning practitioners and scientists. This article introduces objectives and elements of the mentoring program being considered a strategic talent development in a network of excellence. Results from a survey among the mentees and mentors of five subsequent years are presented revealing the principal verification of the program with its main elements: one-by-one mentoring for one year each, joint events, qualification classes for the mentees, projects by mentees and support with publications, and a final certificate. The survey reveals the need for several modifications, such as the introduction of target agreements at the beginning of a mentoring period, the modification of the project study as well as the extension of the mentoring period, which are discussed in detail. Finally, conclusions are drawn regarding the program efficacy and transfer

Luftreinhalte- und Lärmminderungsplanung

Für Luftreinhalte- und Lärmminderungsplanung werden Rechtsgrundlagen, Formen, Aufgaben und Inhalte, Maßnahmen und Verfahrensaspekte wie behördeninterne Kooperationen, ihr Verhältnis zu anderen Planungen und die Öffentlichkeitsbeteiligung vorgestellt und reflektiert

Stadtökologische Traditionslinien

"Ausgehend von einer historischen Analyse der Entwicklungslinien von stadtökologischer Forschung werden im internationalen Vergleich Ansätze zur Stadtökologie miteinander verglichen. Die dabei angewendete, einerseits historisch-analytische und andererseits geographisch differenzierte, Betrachtungsweise, soll schließlich die unterschiedlichen Blickrichtungen auf Stadtökologie (einschließlich der soziologisch-humanökologischen Perspektive) miteinander verbinden. Die älteste Traditionslinie der Stadtökologie geht auf naturhistorische Forschungsmethoden zurück, die zunächst in der sogenannten freien Landschaft sowie in Wäldern und Urwäldern erprobt und die später innerhalb von Städten angewendet wurden. In den 1920er Jahren etablierte sich in Chicago eine soziologisch-humanökologische Entwicklungslinie von Stadtökologie, die nicht Tiere und Pflanzen, sondern den Mensch ins Zentrum des Interesses rückte. Chicago hatte eine rasante Entwicklung von einer durch agrarische Tätigkeit geprägte Stadt zur industriell geprägten Großstadt hinter sich. In den 1970er Jahren wurde von Herbert Sukopp gemeinsam mit weiteren Professoren der TU Berlin ein komplexer Ansatz entwickelt, der im Theoriekern Stadtökologie als Disziplin bio-ökologischer Zugehörigkeit definiert. Dieser deutlich standortkundlich geprägte Ansatz knüpft teilweise an die naturhistorisch-ökologische Traditionslinie an. Ebenfals in den 1970er Jahren des vergangenen Jahrhunderts entstand ein Zweig stadtökologischer Forschung, der Stoffflüsse und Energieflüsse in Städten zum Forschungsobjekt machte. In diese Phase fällt 'die Ölkrise'. Etwa zwanzig Jahre später wurden zunehmend Nachhaltigkeitsaspekte bei stadtökologischen Forschungsfragen berücksichtigt, wobei die Folgen der Globalisierung zunehmend reflektiert werden. Heute bestehen verschiedene Traditionslinien zur Stadtökologie mit- und nebeneinander fort. 'Nachhaltigkeit' als Leitbild kann alle Traditionslinien zur Stadtökologie integrieren, geht jedoch darüber hinaus. Zudem bestehen zwischen Vertretern der unterschiedlichen Traditionslinien Zielkonflikte bei konkreten Planungssituationen. International ist festzustellen, dass sich im Zuge der Globalisierung im Vergleich der Industrienationen die stadtökologische Forschung zunehmend einander angleicht. Die dominanten Forschungsthemen variieren aber stark je nach den jeweiligen länderspezifischen Problemen und Wertvorstellungen." (Autorenreferat

A comparison of consistent UV treatment versus inconsistent UV treatment in horticultural production of lettuce

UV radiation is an underrated radiation currently missing in many horticultural production systems of vegetables in protected cultivation. It can be added e.g., in LED light sources. Using lettuce as a model plant, this study determined whether the use of UVB LEDs is suitable (1) for use in consistent systems (indoor farming) or (2) inconsistent systems (greenhouse). Blue and red LEDs were selected as additional artificial lighting to UVB LEDs. Both approaches led to a reproducible increase of desired flavonol glycosides, such as quercetin-3-O-(6′′-O-malonyl)-glucoside or quercetin-3-O-glucuronide and the anthocyanin cyanidin-3-O-(6′′-O-malonyl)-glucoside in lettuce. The impact of the consistent UVB treatment is higher with up to tenfold changes than that of the inconsistent UVB treatment in the greenhouse. Varying natural light and temperature conditions in greenhouses might affect the efficiency of the artificial UVB treatment. Here, UVB LEDs have been tested and can be recommended for further development of lighting systems in indoor farming and greenhouse approaches

Clinical and genetic features of amyotrophic lateral sclerosis patients with C9orf72 mutations

An expansion of the GGGGCC hexanucleotide in the non-coding region of C9orf72 represents the most common cause of familial amyotrophic lateral sclerosis. The objective was to describe and analyse the clinical and genetic features of amyotrophic lateral sclerosis patients with C9orf72 mutations in a large population. Between November 2011 and December 2020, clinical and genetic characteristics of n = 248 patients with amyotrophic lateral sclerosis carrying C9orf72 mutations were collected from the clinical and scientific network of German motoneuron disease centres. Clinical parameters included age of onset, diagnostic delay, family history, neuropsychological examination, progression rate, phosphorylated neurofilament heavy chain levels in CSF and survival. The number of repeats was correlated with the clinical phenotype. The clinical phenotype was compared to n = 84 patients with SOD1 mutations and n = 2178 sporadic patients without any known disease-related mutations. Patients with C9orf72 featured an almost balanced sex ratio with 48.4% (n = 120) women and 51.6% (n = 128) men. The rate of 33.9% patients (n = 63) with bulbar onset was significantly higher compared to sporadic (23.4%, P = 0.002) and SOD1 patients (3.1%, P < 0.001). Of note, 56.3% (n = 138) of C9orf72, but only 16.1% of SOD1 patients reported a negative family history (P < 0.001). The GGGGCC hexanucleotide repeat length did not influence the clinical phenotypes. Age of onset (58.0, interquartile range 52.0-63.8) was later compared to SOD1 (50.0, interquartile range 41.0-58.0;P < 0.001), but earlier compared to sporadic patients (61.0, interquartile range 52.0-69.0;P = 0.01). Median survival was shorter (38.0 months) compared to SOD1 (198.0 months, hazard ratio 1.97, 95% confidence interval 1.34-2.88;P < 0.001) and sporadic patients (76.0 months, hazard ratio 2.34, 95% confidence interval 1.64-3.34;P < 0.001). Phosphorylated neurofilament heavy chain levels in CSF (2880, interquartile range 1632-4638 pg/ml) were higher compared to sporadic patients (1382, interquartile range 458-2839 pg/ml;P < 0.001). In neuropsychological screening, C9orf72 patients displayed abnormal results in memory, verbal fluency and executive functions, showing generally worse performances compared to SOD1 and sporadic patients and a higher share with suspected frontotemporal dementia. In summary, clinical features of patients with C9orf72 mutations differ significantly from SOD1 and sporadic patients. Specifically, they feature a more frequent bulbar onset, a higher share of female patients and shorter survival. Interestingly, we found a high proportion of patients with negative family history and no evidence of a relationship between repeat lengths and disease severity. Wiesenfarth et al. report that amyotrophic lateral sclerosis patients with C9orf72 mutations differ significantly from sporadic patients and SOD1 gene carriers, including a higher share of bulbar onset, female patients, more severe neuropsychological deficits and shorter survival. No evidence of a relationship between repeat lengths and disease severity was found