The regional weed vegetation in organic spring-sown cereals as shaped by local management, crop diversity and site

Bundesweit hat Mecklenburg Vorpommern einen sehr hohen Anteil an Ökologischer Landwirtschaft. Nach wie vor sind Unkräuter eine Herausforderung in diesen Agrarsystemen. Agrobiodiversität zu fördern, hat in Deutschland einen zunehmenden Stellenwert. Vor diesem Hintergrund sollten Unkräuter einerseits in langfristig handhabbaren Größenordnungen bleiben, andererseits aber auch eine artenreiche Flora bilden. Unser Ziel ist es, zu untersuchen, ob diese beiden Aspekte durch ein vielseitiges Management der Kulturpflanzen unterstützt werden können. Dafür wurden Unkraut und Management Daten von Sommergetreideflächen ökologisch wirtschaftender Betriebe in Mecklenburg-Vorpommern über zwei Jahre (2015-2016) erfasst. Die Auswirkungen von lokalen Umwelt- und Management-Faktoren auf die Unkrautgemeinschaften wurden multivariat analysiert und im Anschluss wurden Effekte der Variablen zur Kulturvielfalt separat untersucht. Wir fanden grundlegende Unterschiede in den Einflüssen des kurzfristigen Anbaumanagements, der langfristigen Kulturvielfaltsstrategien und den eher beständigen Standortfaktoren. Während Unkrautdichten vor allem durch direktes Management beeinflusst werden, verändern sich Unkrautartenvielfalt und –gemeinschaften, wenn Maßnahmen der Kulturvielfalt angewendet werden.Mecklenburg Vorpommern has one of the highest percentages of organic arable production nationwide. Weeds remain to be the main challenge within this agricultural system. There is also an increase in the national support of agrobiodiversity. Weeds should therefore be continuously kept within manageable limits, while on the other side encourage a specie rich weed flora. Our objective is to investigate to which extent these two aspects can be addressed through the use of diversified crop management. In order to research this objective, weed and management data of spring sown cereal crops were obtained from organic farms in the region over the course of two years (2015-2016). The impact of the local environment and management factors on the occurring weed communities was studied in multivariate analysis approaches, followed by the separate crop diversity effects. We found a fundamental difference between the workings of the short-term management, the long-term crop diversification strategies and the more continuos site variables on the weed vegetation. Weed densities were mostly affected by direct management, while weed diversity and communities were altered through the application of crop diversity variables

Acyl Ghrelin Improves Synapse Recovery in an In Vitro Model of Postanoxic Encephalopathy

Comatose patients after cardiac arrest have a poor prognosis. Approximately half never awakes as a result of severe diffuse postanoxic encephalopathy. Several neuroprotective agents have been tested, however without significant effect. In the present study, we used cultured neuronal networks as a model system to study the general synaptic damage caused by temporary severe hypoxia and the possibility to restrict it by ghrelin treatment. Briefly, we applied hypoxia (pO2 lowered from 150 to 20 mmHg) during 6 h in 55 cultures. Three hours after restoration of normoxia, half of the cultures were treated with ghrelin for 24 h, while the other, non-supplemented, were used as a control. All cultures were processed immunocytochemically for detection of the synaptic marker synaptophysin. We observed that hypoxia led to drastic decline of the number of synapses, followed by some recovery after return to normoxia, but still below the prehypoxic level. Additionally, synaptic vulnerability was selective: large- and small-sized neurons were more susceptible to synaptic damage than the medium-sized ones. Ghrelin treatment significantly increased the synapse density, as compared with the non-treated controls or with the prehypoxic period. The effect was detected in all neuronal subtypes. In conclusion, exogenous ghrelin has a robust impact on the recovery of cortical synapses after hypoxia. It raises the possibility that ghrelin or its analogs may have a therapeutic potential for treatment of postanoxic encephalopathy

Omineca Herald, July, 10, 1914

Patients admitted to an intensive care unit after cardiac arrest often suffer from severe brain injury. This injury worsens further after restoration of circulation due to the cascade of reactions in the brain. Neuroprotective therapies aim to diminish this secondary brain injury, thereby targeting at a better outcome. Several new large international studies will start soon, next to two smaller national phase II studies. In this paper we describe the new studies and invite Dutch intensive care units to join

Why Are Sensory Axons More Vulnerable for Ischemia than Motor Axons?

Objective:In common peripheral neuropathies, sensory symptoms usually prevail over motor symptoms. This predominance of sensory symptoms may result from higher sensitivity of sensory axons to ischemia.Methods:We measured median nerve compound sensory action potentials (CSAPs), compound muscle action potentials (CMAPs), and excitability indices in five healthy subjects during forearm ischemia lasting up to disappearance of both CSAPs and CMAPs.Results:Ischemia induced: (1) earlier disappearance of CSAPs than CMAPs (mean ± standard deviation 30±5 vs. 46±6 minutes), (2) initial changes compatible with axonal depolarization on excitability testing (decrease in threshold, increase in strength duration time constant (SDTC) and refractory period, and decrease in absolute superexcitability) which were all more prominent in sensory than in motor axons, and (3) a subsequent decrease of SDTC reflecting a decrease in persistent Na+ conductance during continuing depolarisation.Interpretation:Our study shows that peripheral sensory axons are more vulnerable for ischemia than motor axons, with faster inexcitability during ischemia. Excitability studies during ischemia showed that this was associated with faster depolarization and faster persistent Na+ channel inactivation in sensory than in motor axons. These findings might be attributed to differences in ion channel composition between sensory and motor axons and may contribute to the predominance of sensory over motor symptoms in common peripheral neuropathies. © 2013 Hofmeijer et al

Architectures for wireless sensor networks

The vision of ubiquitous computing requires the development of devices and technologies that can be pervasive without being intrusive. The basic component of such a smart environment will be a small node with sensing and wireless communications capabilities, able to organize itself flexibly into a network for data collection and delivery. Building such a sensor network presents many significant challenges, especially at the architectural, protocol, and operating system level. Although sensor nodes might be equipped with a power supply or energy scavenging means and an embedded processor that makes them autonomous and self-aware, their functionality and capabilities will be very limited. Therefore, collaboration between nodes is essential to deliver smart services in a ubiquitous setting. New algorithms for networking and distributed collaboration need to be developed. These algorithms will be the key for building self-organizing and collaborative sensor networks that show emergent behavior and can operate in a challenging environment where nodes move, fail, and energy is a scarce resource. The question that rises is how to organize the internal software and hardware components in a manner thatwill allowthem towork properly and be able to adapt dynamically to new environments, requirements, and applications. At the same time the solution should be general enough to be suited for as many applications as possible. Architecture definition also includes, at the higher level, a global view of the whole network. The topology, placement of base stations, beacons, etc. is also of interest. In this chapter, we will present and analyze some of the characteristics of the architectures for wireless sensor networks. Then, we will propose a new dataflow-based architecture that allows, as a new feature, the dynamic reconfiguration of the sensor nodes software at runtime

Unstandardized Treatment of Electroencephalographic Status Epilepticus Does Not Improve Outcome of Comatose Patients after Cardiac Arrest

Objective: Electroencephalographic status epilepticus occurs in 9–35% of comatose patients after cardiac arrest. Mortality is 90–100%. It is unclear whether (some) seizure patterns represent a condition in which anti-epileptic treatment may improve outcome, or severe ischemic damage, in which treatment is futile. We explored current treatment practice and its effect on patients’ outcome. Methods: We retrospectively identified patients that were treated with anti-epileptic drugs from our prospective cohort study on the value of continuous electroencephalography (EEG) in comatose patients after cardiac arrest. Outcome at 6 months was dichotomized between “good” [cerebral performance category (CPC) 1 or 2] and “poor” (CPC 3, 4, or 5). EEG analyses were done at 24 h after cardiac arrest and during anti-epileptic treatment. Unequivocal seizures and generalized periodic discharges during more than 30 min were classified as status epilepticus. Results: Thirty-one (22%) out of 139 patients were treated with anti-epileptic drugs (phenytoin, levetiracetam, valproate, clonazepam, propofol, midazolam), of whom 24 had status epilepticus. Dosages were moderate, barbiturates were not used, medication induced burst-suppression not achieved, and treatment improved electroencephalographic status epilepticus patterns temporarily (<6 h). Twenty-three patients treated for status epilepticus (96%) died. In patients with status epilepticus at 24 h, there was no difference in outcome between those treated with and without anti-epileptic drugs. Conclusion: In comatose patients after cardiac arrest complicated by electroencephalographic status epilepticus, current practice includes unstandardized, moderate treatment with anti-epileptic drugs. Although widely used, this does probably not improve patients’ outcome. A randomized controlled trial to estimate the effect of standardized, aggressive treatment, directed at complete suppression of epileptiform activity during at least 24 h, is needed and in preparation