Predation of cockles (Cerastoderma edule) by the whelk (Buccinum undatum) under laboratory conditions

The feeding rate and behaviour of whelks (Buccinum undatum) offered cockles (Cerastoderma edule) in laboratory experiments were examined. When presented with cockles in a range of sizes (10–40 mm), 14 B. undatum (34.6–88.3 mm), held individually in aquaria, consumed a wide size range of cockles. Small whelks (\u3c40 \u3emm) consumed cockles (\u3c23 \u3emm), whereas large whelks, (\u3e60 mm) ate a greater number of larger cockles (\u3e30 mm) and a wider size range of cockles (12–40 mm) than smaller whelks. The majority (90%) of the shells of the predated cockles were undamaged and the few (B. undatum feeding on C. edule showed a method of attack that has not previously been reported and involved the use of the whelk\u27s foot to asphyxiate the cockle or to pull the shell valves apart. No filmed evidence was found for the previously reported shell ‘wedging’ technique for prising open the closed shell valves of C. edule, although 10% of the shells of consumed cockles in feeding experiments had damaged shell margins

Mechanisms of Oxidative Damage in Multiple Sclerosis and a Cell Therapy Approach to Treatment

Although significant advances have recently been made in the understanding and treatment of multiple sclerosis, reduction of long-term disability remains a key goal. Evidence suggests that inflammation and oxidative stress within the central nervous system are major causes of ongoing tissue damage in the disease. Invading inflammatory cells, as well as resident central nervous system cells, release a number of reactive oxygen and nitrogen species which cause demyelination and axonal destruction, the pathological hallmarks of multiple sclerosis. Reduction in oxidative damage is an important therapeutic strategy to slow or halt disease processes. Many drugs in clinical practice or currently in trial target this mechanism. Cell-based therapies offer an alternative source of antioxidant capability. Classically thought of as being important for myelin or cell replacement in multiple sclerosis, stem cells may, however, have a more important role as providers of supporting factors or direct attenuators of the disease. In this paper we focus on the antioxidant properties of mesenchymal stem cells and discuss their potential importance as a cell-based therapy for multiple sclerosis

Percutaneous Endoscopic Gastrostomy Tube Insertion in Neurodegenerative Disease:a Retrospective Study and Literature Review

Background/Aims With the notable exceptions of dementia, stroke, and motor neuron disease, relatively little is known about the safety and utility of percutaneous endoscopic gastrostomy (PEG) tube insertion in patients with neurodegenerative disease. We aimed to determine the safety and utility of PEG feeding in the context of neurodegenerative disease and to complete a literature review in order to identify whether particular factors need to be considered to improve safety and outcome. Methods A retrospective case note review of patients referred for PEG insertion by neurologists in a single neuroscience center was conducted according to a pre-determined set of standards. For the literature review, we identified references from searches of PubMed, mainly with the search items “percutaneous endoscopic gastrostomy” and “neurology” or “neurodegenerative disease.” Results Short-term mortality and morbidity associated with PEG in patients with neurological disease were significant. Age greater than 75 years was associated with poor outcome, and a trend toward adverse outcome was observed in patients with low serum albumin. Conclusions This study highlights the relatively high risk of PEG in patients with neurodegenerative disease. We present points for consideration to improve outcome in this particularly vulnerable group of patients

Purkinje cell injury, structural plasticity and fusion in patients with Friedreich's ataxia

Purkinje cell pathology is a common finding in a range of inherited and acquired cerebellar disorders, with the degree of Purkinje cell injury dependent on the underlying aetiology. Purkinje cells have an unparalleled resistance to insult and display unique regenerative capabilities within the central nervous system. Their response to cell injury is not typical of most neurons and likely represents both degenerative, compensatory and regenerative mechanisms. Here we present a pathological study showing novel and fundamental insights into Purkinje cell injury, remodelling and repair in Friedreich’s ataxia; the most common inherited ataxia. Analysing post-mortem cerebellum tissue from patients who had Friedreich's ataxia, we provide evidence of significant injury to the Purkinje cell axonal compartment with relative preservation of both the perikaryon and its extensive dendritic arborisation. Axonal remodelling of Purkinje cells was clearly elevated in the disease. For the first time in a genetic condition, we have also shown a disease-related increase in the frequency of Purkinje cell fusion and heterokaryon formation in Friedreich's ataxia cases; with evidence that underlying levels of cerebellar inflammation influence heterokaryon formation. Our results together further demonstrate the Purkinje cell’s unique plasticity and regenerative potential. Elucidating the biological mechanisms behind these phenomena could have significant clinical implications for manipulating neuronal repair in response to neurological injury

Erdheim Chester disease – 25 year history with early CNS involvement

We report a case of Erdheim-Chester disease (ECD) with a 25-year history following initial presentation with diabetes insipidus and brainstem involvement. The exceptionally long history is particularly notable, given that ECD is a life-threatening disorder and there is a recognised association between central nervous system involvement and poor outcome. The case is a timely reminder of the presenting features of the condition, given the emergence of potential new treatment options