Höhere Qualität von Lebensmitteln durch gesetzlich geschützte Herkunftsangaben

Die Qualität von Lebensmitteln - insbesondere im Hinblick auf die Güte der Inhaltsstoffe und die Herstellungsart - ist von Verbrauchern nur schwer überprüfbar. Um die Glaubwürdigkeit von Qualitätsversprechen zu erhöhen und die Unsicherheit in der Beziehung zwischen Herstellern und Verbrauchern zu reduzieren, können Vereinigungen von Lebensmittelproduzenten seit 1992 Herkunftsangaben bei der Europäischen Union schützen lassen. Die Untersuchung zeigt, dass Produkte mit geschützter Herkunft höhere Preise auf Endverbrauchermärkten erzielen. Dies ist ein klares Indiz dafür, dass durch den Schutz von Herkunftsangaben tatsächlich eine höhere Glaubwürdigkeit von Qualitätsversprechen erreicht wird. Qualitätsorientierte Verbraucher sind unter diesen Bedingungen bereit, mehr zu zahlen. Deutlich wird allerdings auch, dass der gesetzliche Herkunftsschutz Monopolisierungstendenzen auf der Herstellerseite begünstigt. Solch negative Auswirkungen können zum Teil vermieden werden, wenn allein traditionelle Herstellungsverfahren, nicht aber die regionale Herkunft, geschützt würden.Asymmetric Information, Protected designation of origin, Product differentiation

Einfluss dekompressiver Kraniektomie und fokaler Hypothermie auf die neurologische Langzeitfunktion in einem Mausmodell des geschlossenen Schädel-Hirn-Traumas

Das Schädel-Hirn-Trauma zählt zu den häufigsten Ursachen für Tod und bleibende Behinderung weltweit. In der vorliegenden Arbeit sollen die Auswirkungen einer dekompressiven Kraniektomie alleine und in Kombination mit nachfolgender Anwendung therapeutischer fokaler Hypothermie auf die langfristige neurologische Funktion nach Schädel-Hirn-Trauma evaluiert werden. Weiterhin wird der Einfluss dieser beiden Therapieoptionen auf strukturellen Hirnschaden, Neuronenverlust, Hirnödembildung, Neuroinflammation und Apoptose diskutiert. Die Versuchstiere – Mäuse der Rasse CD-1 – wurden hierfür in fünf Versuchsgruppen mit einer Gruppengröße von jeweils acht Tieren randomisiert: Sham-Gruppe, Kontrollgruppe ohne Trauma mit Kraniektomie, Kontrollgruppe mit Trauma ohne Therapie, Therapiegruppe mit Trauma und Kraniektomie, Therapiegruppe mit Trauma, Kraniektomie und fokaler Hypothermie. Die Applikation eines mittelschweren, geschlossenen Schädel-Hirn-Traumas erfolgte durch ein etabliertes, standardisiertes Modell (weight drop - Modell). Im Anschluss wurden in den entsprechenden Gruppen eine dekompressive temporoparietale Hemikraniektomie durchgeführt und milde fokale Hypothermie (Zieltemperatur 32 °C) über eine Kühlsonde appliziert. Eine neurologische Verlaufsbeurteilung wurde durch die Erhebung des Neurological Severity Score, des Beam Balance Score und der Beam Balance Time an den postoperativen Tagen 1, 3, 7, 14 und 28 angeschlossen. Nach Ablauf des Untersuchungszeitraums erfolgte die Euthanasie durch intrakardiale Formaldehydperfusion und die Präparation des Gehirns. Anhand der histologischen Standardfärbungen Hämatoxilin – Eosin und Nissl wurden struktureller Hirnschaden und hippocampaler Neuronenverlust beurteilt. Zur Beurteilung von Hirnödembildung, Neuroinflammation und Apoptose schloss sich die Auswertung immunhistochemischer Anfärbungen der Strukturen Aquaporin – 4, saures Gliafaserprotein und Bcl-2 an. Folge dekompressiver Kraniektomie in der vorliegenden Arbeit ist eine signifikant verschlechterte neurologische Langzeitfunktion. Die zusätzliche Anwendung fokaler Hypothermie führt zu einem Ausgleich dieses negativen Effektes zugunsten einer verbesserten neurologischen Funktion. Zusätzlich führt die Anwendung fokaler Hypothermie im Vergleich zur alleinigen Dekompression zu einer deutlichen Mortalitätsreduktion im Verlauf. In der histologischen Auswertung zeigen sich struktureller Hirnschaden, Hirnödemformation und Neuroinflammation unbeeinflusst von den durchgeführten Therapieoptionen. In allen Gruppen mit Schädel-Hirn-Trauma ist eine unspezifische Erhöhung der Expression von Aquaporin-4 und saurem Gliafaserprotein nachweisbar. Ein hippocampaler Neuronenverlust liegt nicht vor. Dekompressive Kraniektomie führt zu einer verminderten Expression von antiapoptotisch wirksamem Bcl-2. Durch die zusätzliche Anwendung fokaler Hypothermie folgt 5 eine hoch signifikant vermehrte Expression von Bcl-2, vereinbar mit vorbeschriebenen antiapoptotischen, neuroprotektiven Effekten milder Hypothermie. Die vorliegende Arbeit ergänzt die aktuelle Diskussion über die Anwendung dekompressiver Kraniektomie und therapeutischer Hypothermie nach Schädel-Hirn-Trauma. Um die dargestellten positiven Auswirkungen fokaler Hypothermie in einem kombinierten Verfahren mit dekompressiver Kraniektomie beim Menschen zu verifizieren, benötigt es randomisierter, klinischer Studien.Traumatic brain injury is one of the leading causes of death and disability worldwide. The aim of this study is to evaluate the influence of decompressive temporoparietal hemicraniectomy and the subsequent application of therapeutic focal hypothermia on neurologic impairment in a long-term closed head injury model. Furthermore, the influence of these therapeutic options on structural brain damage, neuronal loss, brain oedema formation, neuroinflammation and apoptosis will be discussed. Laboratory animals – CD-1 mice – were randomized in five experimental groups with the size of eight animals each: Sham, craniectomy without trauma, trauma without therapy, trauma with craniectomy, trauma with craniectomy and subsequent focal hypothermia. Moderate Closed Head Injury was applied using an established weight drop model. Thereafter decompressive temporoparietal craniectomy was performed and subsequent mild focal hypothermia (32°C) was applied. Neurological assessment followed on posttraumatic time points 1, 3, 7, 14 and 28 days by performance of Neurological Severity Score, Beam Balance Score and Beam Balance Time. After 28 days animals were sacrificed via intracardial perfusion of formaldehyde. Brain preparation and histological and immunohistochemical staining followed. Standard haematoxylin and eosin as well as Nissl staining were used to analyse structural brain damage and neuronal loss in the hippocampus. Oedema formation, neuroinflammation and apoptosis were evaluated by assessment of immunohistochemical staining of Aquaporin-4, glial fibrillary acidic protein and Bcl-2. In this study, the performance of decompressive craniectomy is followed by significant neurological impairment. Subsequent application of focal hypothermia diminishes this negative effect. Additional, therapeutic focal hypothermia reduces mortality compared to sole decompression. Histological assessment showed no influence of decompression or focal hypothermia on structural brain damage, neuroinflammation or brain oedema formation. Posttraumatic elevation of immunohistochemical markers Aquaporin-4 and glial fibrillary acidic protein remained unaltered by therapy. No neuronal loss could be detected in the hippocampus. Antiapoptotic Bcl-2 was elevated following decompressive craniectomy. Subsequent focal hypothermia led to further, highly significant increase of Bcl-2, consistent with previously described antiapoptotic, neuroprotective effects of mild hypothermia. This study adds to the present debate about decompressive craniectomy and therapeutic hypothermia after traumatic brain injury. To verify these positive effects of focal hypothermia subsequent to decompressive craniectomy in humans, controlled randomized clinical trials will be necessary

Severe Traumatic Brain Injury in children—paradigm of decompressive craniectomy compared to a historic cohort

Purpose Traumatic brain injury (TBI) is one of the leading causes of death and disability in children. Medical therapy remains limited, and decompressive craniectomy (DC) is an established rescue therapy in case of elevated intracranial pressure (ICP). Much discussion deals with clinical outcome after severe TBI treated with DC, while data on the pediatric population is rare. We report our experience of treating severe TBI in two different treatment setups at the same academic institution. Methods Forty-eight patients (<= 16 years) were hospitalized with severe TBI (GCS <= 8 points) between 2008 and 2018 in a pediatric intensive care unit (ICU) at a specialized tertiary pediatric care center. Data on treatment, clinical status, and outcome was retrospectively analyzed. Outcome data included Glasgow Outcome Scale (GOS) at 3-, 12-, and 36-month follow-up. Data was compared to a historic cohort with 53 pediatric severe TBI patients treated at the same institution in a neurointensive care unit between 1996 and 2007. Ethical approval was granted (EA2/076/21). Results Between 2008 and 2018, 11 patients were treated with DC. Compared to the historic cohort, patients were younger and GCS was worse, while in-hospital mortality and clinical outcome remained similar. A trend towards more aggressive EVD placement and the internal paradigm change for treatment in a specialized pediatric ICU was observed. Conclusions In children with severe TBI treated over two decades, clinical outcome was comparable and mostly favorable in two different treatment setups. Consequent therapy is warranted to maintain the positive potential for favorable outcome in children with severe TBI

Brain Edema Formation and Functional Outcome After Surgical Decompression in Murine Closed Head Injury Are Modulated by Acetazolamide Administration

Acetazolamide (ACZ), carbonic anhydrase inhibitor, has been successfully applied in several neurosurgical conditions for diagnostic or therapeutic purposes. Furthermore, neuroprotective and anti-edematous properties of ACZ have been postulated. However, its use in traumatic brain injury (TBI) is limited, since ACZ-caused vasodilatation according to the Monro-Kellie doctrine may lead to increased intracranial blood volume / raise of intracranial pressure. We hypothesized that these negative effects of ACZ will be reduced or prevented, if the drug is administered after already performed decompression. To test this hypothesis, we used a mouse model of closed head injury (CHI) and decompressive craniectomy (DC). Mice were assigned into following experimental groups: sham, DC, CHI, CHI+ACZ, CHI+DC, and CHI+DC+ACZ (n = 8 each group). 1d and 3d post injury, the neurological function was assessed according to Neurological Severity Score (NSS) and Beam Balance Score (BBS). At the same time points, brain edema was quantified by MRI investigations. Functional impairment and edema volume were compared between groups and over time. Among the animals without skull decompression, the group additionally treated with acetazolamide demonstrated the most severe functional impairment. This pattern was reversed among the mice with decompressive craniectomy: CHI+DC treated but not CHI+DC+ACZ treated animals showed a significant neurological deficit. Accordingly, radiological assessment revealed most severe edema formation in the CHI+DC group while in CHI+DC+ACZ animals, volume of brain edema did not differ from DC-only animals. In our CHI model, the response to acetazolamide treatment varies between animals with decompressive craniectomy and those without surgical treatment. Opening the cranial vault potentially creates an opportunity for acetazolamide to exert its beneficial effects while vasodilatation-related risks are attenuated. Therefore, we recommend further exploration of this potentially beneficial drug in translational research projects

Brain Edema Formation and Functional Outcome After Surgical Decompression in Murine Closed Head Injury Are Modulated by Acetazolamide Administration

Acetazolamide (ACZ), carbonic anhydrase inhibitor, has been successfully applied in several neurosurgical conditions for diagnostic or therapeutic purposes. Furthermore, neuroprotective and anti-edematous properties of ACZ have been postulated. However, its use in traumatic brain injury (TBI) is limited, since ACZ-caused vasodilatation according to the Monro-Kellie doctrine may lead to increased intracranial blood volume / raise of intracranial pressure. We hypothesized that these negative effects of ACZ will be reduced or prevented, if the drug is administered after already performed decompression. To test this hypothesis, we used a mouse model of closed head injury (CHI) and decompressive craniectomy (DC). Mice were assigned into following experimental groups: sham, DC, CHI, CHI+ACZ, CHI+DC, and CHI+DC+ACZ (n = 8 each group). 1d and 3d post injury, the neurological function was assessed according to Neurological Severity Score (NSS) and Beam Balance Score (BBS). At the same time points, brain edema was quantified by MRI investigations. Functional impairment and edema volume were compared between groups and over time. Among the animals without skull decompression, the group additionally treated with acetazolamide demonstrated the most severe functional impairment. This pattern was reversed among the mice with decompressive craniectomy: CHI+DC treated but not CHI+DC+ACZ treated animals showed a significant neurological deficit. Accordingly, radiological assessment revealed most severe edema formation in the CHI+DC group while in CHI+DC+ACZ animals, volume of brain edema did not differ from DC-only animals. In our CHI model, the response to acetazolamide treatment varies between animals with decompressive craniectomy and those without surgical treatment. Opening the cranial vault potentially creates an opportunity for acetazolamide to exert its beneficial effects while vasodilatation-related risks are attenuated. Therefore, we recommend further exploration of this potentially beneficial drug in translational research projects

Navigation accuracy and assessability of carbon fiber-reinforced PEEK instrumentation with multimodal intraoperative imaging in spinal oncology

Radiolucent carbon-fiber reinforced PEEK (CFRP) implants have helped improve oncological follow-up and radiation therapy. Here, we investigated the performance of 3D intraoperative imaging and navigation systems for instrumentation and precision assessment of CFRP pedicle screws across the thoraco-lumbar spine. Thirty-three patients with spinal tumors underwent navigated CFRP instrumentation with intraoperative CT (iCT), robotic cone-beam CT (rCBCT) or cone-beam CT (CBCT) imaging. Two different navigation systems were used for iCT-/rCBCT- and CBCT-based navigation. Demographic, clinical and outcome data was assessed. Four blinded observers rated image quality, assessability and accuracy of CFRP pedicle screws. Inter-observer reliability was determined with Fleiss` Kappa analysis. Between 2018 and 2021, 243 CFRP screws were implanted (iCT:93, rCBCT: 99, CBCT: 51), of which 13 were non-assessable (iCT: 1, rCBCT: 9, CBCT: 3; *p = 0.0475; iCT vs. rCBCT). Navigation accuracy was highest using iCT (74%), followed by rCBCT (69%) and CBCT (49%) (*p = 0.0064; iCT vs. CBCT and rCBCT vs. CBCT). All observers rated iCT image quality higher than rCBCT/CBCT image quality (*p < 0.01) but relevant pedicle breaches were reliably identified with substantial agreement between all observers regardless of the imaging modality. Navigation accuracy for CFRP pedicle screws was considerably lower than expected from reports on titanium implants and CT may be best for reliable assessment of CFRP materials

Therapeutic Approaches Targeting Vascular Repair After Experimental Spinal Cord Injury: A Systematic Review of the Literature

Traumatic spinal cord injury (SCI) disrupts the spinal cord vasculature resulting in ischemia, amplification of the secondary injury cascade and exacerbation of neural tissue loss. Restoring functional integrity of the microvasculature to prevent neural loss and to promote neural repair is an important challenge and opportunity in SCI research. Herein, we summarize the course of vascular injury and repair following SCI and give a comprehensive overview of current experimental therapeutic approaches targeting spinal cord microvasculature to diminish ischemia and thereby facilitate neural repair and regeneration. A systematic review of the published literature on therapeutic approaches to promote vascular repair after experimental SCI was performed using PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) standards. The MEDLINE databases PubMed, Embase, and OVID MEDLINE were searched using the keywords “spinal cord injury,” “angiogenesis,” “angiogenesis inducing agents,” “tissue engineering,” and “rodent subjects.” A total of 111 studies were identified through the search. Five main therapeutic approaches to diminish hypoxia-ischemia and promote vascular repair were identified as (1) the application of angiogenic factors, (2) genetic engineering, (3) physical stimulation, (4) cell transplantation, and (5) biomaterials carrying various factor delivery. There are different therapeutic approaches with the potential to diminish hypoxia-ischemia and promote vascular repair after experimental SCI. Of note, combinatorial approaches using implanted biomaterials and angiogenic factor delivery appear promising for clinical translation

Clinicians’ perspectives on supporting individuals with severe anorexia nervosa in specialist eating disorder intensive treatment settings during the COVID-19 pandemic

Background: The COVID-19 pandemic has significantly affected intensive treatment settings (i.e., inpatient [IP] and day patient [DP]) in specialist eating disorder services. However, the impact on clinicians working in these services is largely unknown. We therefore explored the perspectives of those supporting individuals with severe anorexia nervosa (AN) in intensive treatment settings during the pandemic. Methods: Between May 2020 and June 2021, we interviewed clinicians (n = 21) who delivered IP and/or DP treatment to patients with severe AN in four specialist eating disorder services in the United Kingdom. Data relating to experiences during COVID-19 were analysed using reflexive thematic analysis. Results: We identified six themes: Disruptions to Routine Treatment; Introduction of Virtual Treatment; Separation from Treatment, Others and the World; Impact on Recovery; Impact on Staff; and Pressure on Referral Pathways. COVID-19 posed significant challenges to IP and DP services: forcing closures, operating with restrictions and virtual treatment, and impacting delivery of essential treatment components, referral pathways, clinician wellbeing, risk management, and patient isolation and recovery trajectories. Opportunities arose, in particular in DP services offering virtual support. Conclusions: COVID-19 challenged the continuation of multidisciplinary treatment. The findings underline the necessity for medical, psychological, practical, and nutritional support, as well as carer involvement and fostering social connections to remain at the forefront of intensive treatment for severe AN. They also emphasise the uncertainty surrounding which intensive treatment may be best suited to which patient when, particularly within the context of virtual DP support

The clinical effectiveness and cost-effectiveness of a ‘stepping into day treatment’ approach versus inpatient treatment as usual for anorexia nervosa in adult specialist eating disorder services (DAISIES trial): a study protocol of a randomised controlled multi-centre open-label parallel group non-inferiority trial

BACKGROUND: Anorexia nervosa (AN) is a serious and disabling mental disorder with a high disease burden. In a proportion of cases, intensive hospital-based treatments, i.e. inpatient or day patient treatment, are required, with day patient treatment often being used as a 'step-down' treatment after a period of inpatient treatment. Demand for such treatment approaches has seen a sharp rise. Despite this, the relative merits of these approaches for patients, their families, and the NHS and wider society are relatively unknown. This paper describes the rationale for, and protocol of, a two-arm multi-centre open-label parallel group non-inferiority randomised controlled trial, evaluating the effectiveness and cost-effectiveness of these two intensive treatments for adults with severe AN: inpatient treatment as usual and a stepped care day patient approach (the combination of day patient treatment with the option of initial inpatient treatment for medical stabilisation). The main aim of this trial is to establish whether, in adults with severe AN, a stepped care day patient approach is non-inferior to inpatient treatment as usual in relation to improving body mass index (BMI) at 12 months post-randomisation. METHODS: 386 patients with a Diagnostic and Statistical Manual 5th edition diagnosis of severe AN or related disorder, with a BMI of ≤16 kg/m2 and in need of intensive treatment will be randomly allocated to either inpatient treatment as usual or a stepped care day patient approach. Patients in both groups will receive treatment until they reach a healthy weight or get as close to this point as possible. Assessments will be conducted at baseline (prior to randomisation), and at 6 and 12 months post-randomisation, with additional monthly symptom monitoring. The primary outcome will be BMI at the 12-month post-randomisation assessment. Other outcomes will include psychosocial adjustment; treatment motivation, expectations and experiences; cost-effectiveness; and carer burden. DISCUSSION: The results of this study will provide a rigorous evaluation of two intensive treatment approaches which will inform future national and international treatment guidelines and service provision