A new fossil species of Procellaria (Aves: Procellariiformes) from the Pliocene of New Zealand

We describe a new Procellaria petrel species from the late Pliocene of Taranaki, New Zealand. The new species is most similar morphologically to the White-Chinned Petrel (P. aequinoctialis), Spectacled Petrel (P. conspicillata) and the Westland Petrel (P. westlandica). Compared with those taxa, the new species has a deeper and shorter premaxilla, longer coracoid and shorter wings, while its legs are a similar size. Today, New Zealand is the centre of global diversity of the genus, with four breeding species. This is the first fossil species of Procellaria to be described from New Zealand, attesting to a reasonably long history of this genus in the region

Pathology Associated with AAV Mediated Expression of Beta Amyloid or C100 in Adult Mouse Hippocampus and Cerebellum

Accumulation of beta amyloid (Ab) in the brain is a primary feature of Alzheimer’s disease (AD) but the exact molecular mechanisms by which Ab exerts its toxic actions are not yet entirely clear. We documented pathological changes 3 and 6 months after localised injection of recombinant, bi-cistronic adeno-associated viral vectors (rAAV2) expressing human Ab40- GFP, Ab42-GFP, C100-GFP or C100V717F-GFP into the hippocampus and cerebellum of 8 week old male mice. Injection of all rAAV2 vectors resulted in wide-spread transduction within the hippocampus and cerebellum, as shown by expression of transgene mRNA and GFP protein. Despite the lack of accumulation of Ab protein after injection with AAV vectors, injection of rAAV2-Ab42-GFP and rAAV2- C100V717F-GFP into the hippocampus resulted in significantly increased microgliosis and altered permeability of the blood brain barrier, the latter revealed by high levels of immunoglobulin G (IgG) around the injection site and the presence of IgG positive cells. In comparison, injection of rAAV2-Ab40-GFP and rAAV2-C100-GFP into the hippocampus resulted in substantially less neuropathology. Injection of rAAV2 vectors into the cerebellum resulted in similar types of pathological changes, but to a lesser degree. The use of viral vectors to express different types of Ab and C100 is a powerful technique with which to examine the direct in vivo consequences of Ab expression in different regions of the mature nervous system and will allow experimentation and analysis of pathological AD-like changes in a broader range of species other than mouse

Introducing NICE guidelines for intravenous fluid therapy into a district general hospital

Peer reviewedPublisher PD

Role of Metalloproteases in the Release of the IL-1 type II Decoy Receptor

The IL-1 type II receptor (decoy RII) is a nonsignaling molecule the only established function of which is to capture IL-1 and prevent it from interacting with signaling receptor. The decoy RII is released in a regulated way from the cell surface. Here, we reported that hydroxamic acid inhibitors of matrix metalloproteases inhibit different pathways of decoy RII release, including the following: (a) the slow (18 h) gene expression-dependent release from monocytes and polymorphonuclear cells exposed to dexamethasone; (b) rapid release (minutes) from myelomonocytic cells exposed to tumor necrosis factor, chemoattractants, or phorbol myristate acetate; (c) phorbol myristate acetate-induced release from decoy RII-transfected fibroblasts and B cells. Inhibition of release was associated with increased surface expression of decoy RII. Inhibitors of other protease classes did not substantially affect release. However, serine protease inhibitors increased the molecular mass of the decoy RII released from polymorphonuclear cells from 45 to 60 kDa. Thus, irrespective of the pathway responsible for release and of the cellular context, matrix metalloproteases, rather than differential splicing, play a key role in production of soluble decoy RII

Observations of Persistent Leonid Meteor Trails. 1. Advection of the Diamond Ring

From a single image of a persistent trail left by a -1.5 magnitude Leonid meteor on November 17, 1998, the relative winds between 92.5 and 98 km altitude are derived, where the altitudes are determined by a sodium lidar. These are converted to true winds 82 sec after the appearance of the meteor by fixing the winds at 98 km to match the results of following the trail with the lidar for twelve minutes. The image and winds reveal a fine example of the effects of a gravity wave having a vertical wavelenth of 5.50 ± 0.02 km, a horizontal wavelength of 2650 ± 60 kin, an intrinsic period of 19.5 ± 0.4 hours, and an observed period of 8.6 ± 0.1 hours. Effects of the gravity wave are still present in the wind field 70 rain later

Meteor Trail Advection Observed During the 1998 Leonid Shower

Sodium resonance lidar observations of meteor trails are reported from the 1998 Leonid shower experimental at the Starfire Optical Range Kirtland Air Force Base, NM (35.0º N, 106.5º W ). The lidar was operating in a spatially scanning mode that allowed tracking for up to one half-hour. Three trails are presented here whose motion allowed inference of radial as well as vector wind components and apparent diffusivities. The winds are derived independently using the narrow linewidth sodium (Na) resonance Doppler lidar technique and are compared with the tracking results

Observations of persistent Leonid meteor trails 3. The ‘‘Glowworm’’

A spectacular, well-observed Leonid meteor of visual magnitude -14.3 appeared on 17 November 1998 and left a lingering trail, dubbed the Glowworm, that was well studied. From a location on Kirtland Air Force Base, near Albuquerque, New Mexico, we obtained CCD images of the trail from 94 to 203 s after the meteor and recorded a video with an intensified camera for even longer. From information obtained with a sodium lidar half an hour after the meteor, we have determined that a gravity wave with a vertical wavelength of 2.4 km was responsible for the right-angled appearance of the trail. The trail ended abruptly at 85 km, and its uppermost altitude may have been no greater than 91 km. We designate the Glowworm a Type I trail: one that is wide (1 km), cloudy in appearance, has high diffusion rates (800m2 s-1), high total line emission rates (1.5 x 1018 photons m-1 s-1), and is optically thicker than Type II trails. The lower parts of the Diamond Ring, another Leonid lingering trail that appeared 38 min earlier than the Glowworm, define the Type II trails, which appear as narrow, optically thinner parallel trails, with low diffusion rates (12 m2 s-1) and total line emission rates (1–3 x 1016 photons m1 s-1). No explanation is offered for the two orders of magnitude difference in these quantities. The Glowworm meteor produced infrasound [ReVelle and Whitaker, 1999], from which a meteoroid mass estimate of 522 g was made. We compare our photometry to a detailed numerical modeling of the shape of the trail and emission from the Glowworm made by Zinn et al. [1999], who find that the largest contributors to emission recorded by our CCD and video cameras are atmospheric O2 vibrational bands. Compared to our measurements, their calculated emission is too high by two orders of magnitude, but since most of O2 emission may be absorbed by atmospheric O2 before it reaches the ground, this may indeed be the primary contributor to the observed flux. Although the calculations of Zinn et al. lead to a hollow cylinder appearance which may be appropriate for the Glowworm, it is not pronounced enough to account for the complete darkness between the parallel structures seen in Type II trails. An upper limit to backscattering from dust of 3.7 x 10-5 of the expected return was found from directing a 180 W copper vapor laser at the Glowworm

Cognitive rehabilitation for attention and memory in people with multiple sclerosis: study protocol for a randomised controlled trial (CRAMMS)

Background People with multiple sclerosis have problems with memory and attention. Cognitive rehabilitation is a structured set of therapeutic activities designed to retrain an individual’s memory and other cognitive functions. Cognitive rehabilitation may be provided to teach people strategies to cope with these problems, in order to reduce the impact on everyday life. The effectiveness of cognitive rehabilitation for people with multiple sclerosis has not been established. Methods This is a multi-centre, randomised controlled trial investigating the clinical and cost-effectiveness of a group-based cognitive rehabilitation programme for attention and memory problems for people with multiple sclerosis. Four hundred people with multiple sclerosis will be randomised from at least four centres. Participants will be eligible if they have memory problems, are 18 to 69 years of age, are able to travel to attend group sessions and give informed consent. Participants will be randomised in a ratio of 6:5 to the group rehabilitation intervention plus usual care or usual care alone. Intervention groups will receive 10 weekly sessions of a manualised cognitive rehabilitation programme. The intervention will include both restitution strategies to retrain impaired attention and memory functions and compensation strategies to enable participants to cope with their cognitive problems. All participants will receive a follow-up questionnaire and an assessment by a research assistant at 6 and 12 months after randomisation. The primary outcome is the Multiple Sclerosis Impact Scale (MSIS) Psychological subscale at 12 months. Secondary outcomes include the Everyday Memory Questionnaire, General Health Questionnaire-30, EQ-5D and a service use questionnaire from participants, and the Everyday Memory Questionnaire-relative version and Carer Strain Index from a relative or friend. The primary analysis will be based on intention to treat. A mixed-model regression analysis of the MSIS Psychological subscale at 12 months will be used to estimate the effect of the group cognitive rehabilitation programme. Discussion The study will provide evidence regarding the clinical and cost-effectiveness of a group-based cognitive rehabilitation programme for attention and memory problems in people with multiple sclerosis. Trial registration: ISRCTN09697576. Registered 14 August 2014