Time Is Brain: The Use of EEG Electrode Caps to Rapidly Diagnose Nonconvulsive Status Epilepticus.

OBJECTIVE: To perform a feasibility pilot study comparing the usefulness of EEG electrode cap versus standard scalp EEG for acquiring emergent EEGs in emergency department, inpatient, and intensive care unit patients. BACKGROUND: Nonconvulsive status epilepticus (NCSE) is a neurological emergency diagnosed exclusively by EEG. Nonconvulsive status epilepticus becomes more resistant to treatment 1 hour after continued seizure activity. EEG technologists are alerted "stat" when there is immediate need for an EEG during oncall hours, yet delays are inevitable. Alternatively, EEG caps can be quickly placed by in-house residents at bedside for assessment. DESIGN/METHODS: EEG caps were compared with standard-of-care "stat" EEGs for 20 patients with suspected NCSE. After the order for a stat EEG was placed, neurology residents were simultaneously alerted and placed an EEG cap prior to the arrival of the on-call out-of-hospital technologist. Both EEG cap recordings and standard EEG recordings were visually reviewed at 10 and 20 minutes in a blinded manner by two electroencephalographers. The timing, accuracy of interpretation, and diagnosis between the two techniques were then compared. RESULTS: Of the 20 adult patients, 70% (14 of 20) of EEG cap recordings were interpretable, whereas 95% (19 of 20) standard EEGs were interpretable; three had findings consistent with NCSE on both the EEG cap and standard EEG recordings. In the time analysis, 16 patients were included. EEG cap placement was significantly more time efficient than an EEG performed by technologist using the usual "stat" EEG protocol, with the median EEG cap electrode placement occurring 86 minutes faster than standard EEG (22.5 minutes vs. 104.5 minutes; P < 0.0001; n = 16). CONCLUSIONS: New rapid EEG recording using improved EEG caps may allow for rapid diagnosis and clinical decision making in suspected NCSE.

The Digital Ageing Atlas: integrating the diversity of age-related changes into a unified resource.

Multiple studies characterizing the human ageing phenotype have been conducted for decades. However, there is no centralized resource in which data on multiple age-related changes are collated. Currently, researchers must consult several sources, including primary publications, in order to obtain age-related data at various levels. To address this and facilitate integrative, system-level studies of ageing we developed the Digital Ageing Atlas (DAA). The DAA is a one-stop collection of human age-related data covering different biological levels (molecular, cellular, physiological, psychological and pathological) that is freely available online (http://ageing-map.org/). Each of the >3000 age-related changes is associated with a specific tissue and has its own page displaying a variety of information, including at least one reference. Age-related changes can also be linked to each other in hierarchical trees to represent different types of relationships. In addition, we developed an intuitive and user-friendly interface that allows searching, browsing and retrieving information in an integrated and interactive fashion. Overall, the DAA offers a new approach to systemizing ageing resources, providing a manually-curated and readily accessible source of age-related changes.

Achieving immortality in the C. elegans germline.

Germline immortality is a topic that has intrigued theoretical biologists interested in aging for over a century. The germ cell lineage can be passed from one generation to the next, indefinitely. In contrast, somatic cells are typically only needed for a single generation and are then discarded. Germ cells may, therefore, harbor rejuvenation mechanisms that enable them to proliferate for eons. Such processes are thought to be either absent from or down-regulated in somatic cells, although cell non-autonomous forms of rejuvenation are formally possible. A thorough description of mechanisms that foster eternal youth in germ cells is lacking. The mysteries of germline immortality are being addressed in the nematode Caenorhabditis elegans by studying mutants that reproduce normally for several generations but eventually become sterile. The mortal germline mutants probably become sterile as a consequence of accumulating various forms of heritable cellular damage. Such mutants are abundant, indicating that several different biochemical pathways are required to rejuvenate the germline. Thus, forward genetics should help to define mechanisms that enable the germline to achieve immortality.

Neurogenesis and aging: FGF-2 and HB-EGF restore neurogenesis in hippocampus and subventricular zone of aged mice.

Neurogenesis, which may contribute to the ability of the adult brain to function normally and adapt to disease, nevertheless declines with advancing age. Adult neurogenesis can be enhanced by administration of growth factors, but whether the aged brain remains responsive to these factors is unknown. We compared the effects of intracerebroventricular fibroblast growth factor (FGF)-2 and heparin-binding epidermal growth factor-like growth factor (HB-EGF) on neurogenesis in the hippocampal dentate subgranular zone (SGZ) and the subventricular zone (SVZ) of young adult (3-month) and aged (20-month) mice. Neurogenesis, measured by labelling with bromodeoxyuridine (BrdU) and by expression of doublecortin, was reduced by approximately 90% in SGZ and by approximately 50% in SVZ of aged mice. HB-EGF increased BrdU labelling in SGZ at 3 months by approximately 60% and at 20 months by approximately 450%, which increased the number of BrdU-labelled cells in SGZ of aged mice to approximately 25% of that in young adults. FGF-2 also stimulated BrdU labelling in SGZ, by approximately 25% at 3 months and by approximately 250% at 20 months, increasing the number of newborn neurones in older mice to approximately 20% of that in younger mice. In SVZ, HB-EGF and FGF-2 increased BrdU incorporation by approximately 140% at 3 months and approximately 170% at 20 months, so the number of BrdU-labelled cells was comparable in untreated 3-month-old and growth factor-treated 20-month-old mice. These results demonstrate that the aged brain retains the capacity to respond to exogenous growth factors with increased neurogenesis, which may have implications for the therapeutic potential of neurogenesis enhancement in age-associated neurological disorders.