OpenRatSLAM : an open source brain-based SLAM system

RatSLAM is a navigation system based on the neural processes underlying navigation in the rodent brain, capable of operating with low resolution monocular image data. Seminal experiments using RatSLAM include mapping an entire suburb with a web camera and a long term robot delivery trial. This paper describes OpenRatSLAM, an open-source version of RatSLAM with bindings to the Robot Operating System framework to leverage advantages such as robot and sensor abstraction, networking, data playback, and visualization. OpenRatSLAM comprises connected ROS nodes to represent RatSLAM’s pose cells, experience map, and local view cells, as well as a fourth node that provides visual odometry estimates. The nodes are described with reference to the RatSLAM model and salient details of the ROS implementation such as topics, messages, parameters, class diagrams, sequence diagrams, and parameter tuning strategies. The performance of the system is demonstrated on three publicly available open-source datasets.

Towards brain-based sensor fusion for navigating robots

Current state of the art robot mapping and navigation systems produce impressive performance under a narrow range of robot platform, sensor and environmental conditions, in contrast to animals such as rats that produce “good enough” maps that enable them to function under an incredible range of situations. In this paper we present a rat-inspired featureless sensor-fusion system that assesses the usefulness of multiple sensor modalities based on their utility and coherence for place recognition during a navigation task, without knowledge as to the type of sensor. We demonstrate the system on a Pioneer robot in indoor and outdoor environments with abrupt lighting changes. Through dynamic weighting of the sensors, the system is able to perform correct place recognition and mapping where the static sensor weighting approach fails.

Use of brain computer interface to drive : preliminary results

This paper reports on the implementation of a non-invasive electroencephalography-based brain-computer interface to control functions of a car in a driving simulator. The system is comprised of a Cleveland Medical Devices BioRadio 150 physiological signal recorder, a MATLAB-based BCI and an OKTAL SCANeR advanced driving experience simulator. The system utilizes steady-state visual-evoked potentials for the BCI paradigm, elicited by frequency-modulated high-power LEDs and recorded with the electrode placement of Oz-Fz with Fz as ground. A three-class online brain-computer interface was developed and interfaced with an advanced driving simulator to control functions of the car, including acceleration and steering. The findings are mainly exploratory but provide an indication of the feasibility and challenges of brain-controlled on-road cars for the future, in addition to a safe, simulated BCI driving environment to use as a foundation for research into overcoming these challenges.

Cytogenetics of primary skin tumors

Skin tumors can arise as a result of cumulative genetic abnormalities, including chromosomal ­aberrations that can be described as either morphological (structural rearrangements) or molecular (copy number variations). Cytogenetic techniques have been used to examine both large and small chromosomal aberrations, and include karyotyping, comparative genomic hybridization, and fluorescence in situ hybridization. This chapter describes the recurrent aberrations associated with skin tumors, such as benign melanocytic nevi, melanoma, basal cell carcinoma, squamous cell carcinoma, actinic (solar) keratosis, Bowen’s disease, keratoacanthoma, Merkel cell carcinoma, dermatofibrosarcoma protuberans, and cutaneous lymphomas, as detected by cytogenetic methodologies. A significant number of genomic aberrations are shared across different subtypes of skin tumors, including structural and numerical alterations of chromosome 1, −3p, +3q, +6, +7, +8q, −9p, +9q, −10, −17p, +17q and +20. Aberrations specific to certain skin cancers have also been detected, and include: loss of 18q in squamous cell carcinoma, but not its precursor, actinic keratosis; loss of 9q22 in sporadic basal cell carcinoma; and translocation involving 17q22 and 22q13 in dermatofibrosarcoma protuberans. These regions contain a number of potential candidate genes that are involved in aspects of cell signaling, proliferation, differentiation, and apoptosis. Cytogenetic methodologies continue to evolve with the advent of array-based comparative genomic hybridization, copy number variation microarrays, and next-generation sequencing. It is envisioned that cytogenetic analysis will continue to be employed for identification and further exploration of novel chromosomal regions and associated genes that drive skin tumorigenesis.

The effect of varied test instructions on neuropsychological performance following mild traumatic brain injury : an investigation of ‘diagnosis threat’

Diagnosis threat is a psychosocial factor that has been proposed to contribute to poor outcomes following mild traumatic brain injury (mTBI). This threat is thought to impair the cognitive test performance of individuals with mTBI because of negative injury stereotypes. University students (N= 45, 62.2% female) with a history of mTBI were randomly allocated to a diagnosis threat (DT, n=15), reduced threat (DT-reduced, n=15) or neutral (n=15) group. The reduced threat condition invoked a positive stereotype (i.e., that people with mTBI can perform well on cognitive tests). All participants were given neutral instructions before they completed baseline tests of: a) objective cognitive function across a number of domains; b) psychological symptoms; and, c) PCS symptoms, including self-reported cognitive and emotional difficulties. Participants then received either neutral, DT or DT-reduced instructions, before repeating the tests. Results were analyzed using separate mixed model ANOVAs; one for each dependent measure. The only significant result was for the 2 X 3 ANOVA on an objective test of attention/working memory, Digit Span, p<.05, such that the DT-reduced group performed better than the other groups, which were not different from each other. Although not consistent with predictions or earlier DT studies, the absence of group differences on most tests fits with several recent DT findings. The results of this study suggest that it is timely to reconsider the role of DT as a unique contributor to poor mTBI outcome.

A metastatic neuroendocrine anaplastic small cell tumor in a patient with multiple endocrine neoplasia type 1 syndrome : assessment of disease status and response to doxorubicin, cyclophosphamide, etoposide chemotherapy through scintigraphic imaging with 111In-pentetreotide

Extrapulmonary small cell and small cell neuroendocrine tumors of unknown primary site are, in general, aggressive neoplasms with a short median survival. Like small cell lung cancer (SCLC), they often are responsive to chemotherapy and radiotherapy. Small cell lung cancer and well differentiated neuroendocrine carcinomas of the gastrointestinal tract and pancreas tend to express somatostatin receptors. These tumors may be localized in patients by scintigraphic imaging using radiolabeled somatostatin analogues. A patient with an anaplastic neuroendocrine small cell tumor arising on a background of multiple endocrine neoplasia type 1 syndrome is reported. The patient had a known large pancreatic gastrinoma and previously treated parathyroid adenopathy. At presentation, there was small cell cancer throughout the liver and skeleton. Imaging with a radiolabeled somatostatin analogue, 111In- pentetreotide (Mallinckrodt Medical B. V., Petten, Holland), revealed all sites of disease detected by routine biochemical and radiologic methods. After six cycles of chemotherapy with doxorubicin, cyclophosphamide, and etoposide, there was almost complete clearance of the metastatic disease. 111In-pentetreotide scintigraphy revealed uptake consistent with small areas of residual disease in the liver, the abdomen (in mesenteric lymph nodes), and posterior thorax (in a rib). The primary gastrinoma present before the onset of the anaplastic small cell cancer showed no evidence of response to the treatment. The patient remained well for 1 year and then relapsed with brain, lung, liver, and skeletal metastases. Despite an initial response to salvage radiotherapy and chemotherapy with carboplatin and dacarbazine, the patient died 6 months later.

Brain-inspired sensor fusion for navigating robots

Current state of the art robot mapping and navigation systems produce impressive performance under a narrow range of robot platform, sensor and environmental conditions, in contrast to animals such as rats that produce “good enough” maps that enable them to function under an incredible range of situations. In this paper we present a rat-inspired featureless sensor-fusion system that assesses the usefulness of multiple sensor modalities based on their utility and coherence for place recognition, without knowledge as to the type of sensor. We demonstrate the system on a Pioneer robot in indoor and outdoor environments with abrupt lighting changes. Through dynamic weighting of the sensors, the system is able to perform correct place recognition and mapping where the static sensor weighting approach fails.

Is recovery driven by central or peripheral factors? A role for the brain in recovery following intermittent-sprint exercise

Prolonged intermittent-sprint exercise (i.e., team sports) induce disturbances in skeletal muscle structure and function that are associated with reduced contractile function, a cascade of inflammatory responses, perceptual soreness, and a delayed return to optimal physical performance. In this context, recovery from exercise-induced fatigue is traditionally treated from a peripheral viewpoint, with the regeneration of muscle physiology and other peripheral factors the target of recovery strategies. The direction of this research narrative on post-exercise recovery differs to the increasing emphasis on the complex interaction between both central and peripheral factors regulating exercise intensity during exercise performance. Given the role of the central nervous system (CNS) in motor-unit recruitment during exercise, it too may have an integral role in post-exercise recovery. Indeed, this hypothesis is indirectly supported by an apparent disconnect in time-course changes in physiological and biochemical markers resultant from exercise and the ensuing recovery of exercise performance. Equally, improvements in perceptual recovery, even withstanding the physiological state of recovery, may interact with both feed-forward/feed-back mechanisms to influence subsequent efforts. Considering the research interest afforded to recovery methodologies designed to hasten the return of homeostasis within the muscle, the limited focus on contributors to post-exercise recovery from CNS origins is somewhat surprising. Based on this context, the current review aims to outline the potential contributions of the brain to performance recovery after strenuous exercise.

Genome-wide DNA methylation analysis of human brain tissue from schizophrenia patients

Recent studies suggest that genetic and environmental factors do not account for all the schizophrenia risk and epigenetics also plays a role in disease susceptibility. DNA methylation is a heritable epigenetic modification that can regulate gene expression. Genome-Wide DNA methylation analysis was performed on post-mortem human brain tissue from 24 patients with schizophrenia and 24 unaffected controls. DNA methylation was assessed at over 485 000 CpG sites using the Illumina Infinium Human Methylation450 Bead Chip. After adjusting for age and post-mortem interval (PMI), 4 641 probes corresponding to 2 929 unique genes were found to be differentially methylated. Of those genes, 1 291 were located in a CpG island and 817 were in a promoter region. These include NOS1, AKT1, DTNBP1, DNMT1, PPP3CC and SOX10 which have previously been associated with schizophrenia. More than 100 of these genes overlap with a previous DNA methylation study of peripheral blood from schizophrenia patients in which 27 000 CpG sites were analysed. Unsupervised clustering analysis of the top 3 000 most variable probes revealed two distinct groups with significantly more people with schizophrenia in cluster one compared to controls (p = 1.74x10-4). The first cluster was composed of 88% of patients with schizophrenia and only 12% controls while the second cluster was composed of 27% of patients with schizophrenia and 73% controls. These results strongly suggest that differential DNA methylation is important in schizophrenia etiology and add support for the use of DNA methylation profiles as a future prognostic indicator of schizophrenia.

The effect of varying diagnostic terminology within patient discharge information on expected mild traumatic brain injury outcome

This study aimed to determine if systematic variation of the diagnostic terminology embedded within written discharge information (i.e., concussion or mild traumatic brain injury, mTBI) would produce different expected symptoms and illness perceptions. We hypothesized that compared to concussion advice, mTBI advice would be associated with worse outcomes. Sixty-two volunteers with no history of brain injury or neurological disease were randomly allocated to one of two conditions in which they read a mTBI vignette followed by information that varied only by use of the embedded terms concussion (n = 28) or mTBI (n = 34). Both groups reported illness perceptions (timeline and consequences subscale of the Illness Perception Questionnaire-Revised) and expected Postconcussion Syndrome (PCS) symptoms 6 months post injury (Neurobehavioral Symptom Inventory, NSI). Statistically significant group differences due to terminology were found on selected NSI scores (i.e., total, cognitive and sensory symptom cluster scores (concussion > mTBI)), but there was no effect of terminology on illness perception. When embedded in discharge advice, diagnostic terminology affects some but not all expected outcomes. Given that such expectations are a known contributor to poor mTBI outcome, clinicians should consider the potential impact of varied terminology on their patients.

Investigation of brain derived neurotrophic factor (BDNF) gene variants in migraine

A number of observations have suggested that brain derived neurotrophic factor (BDNF) plays a role in migraine pathophysiology. This study investigates whether variants in the BDNF gene are associated with migraine in an Australian case-control population. Background. Brain derived neurotrophic factor (BDNF) has an important role in neural growth, development and survival in the central nervous system and is an important modulator of central and peripheral pain responses. Variants in BDNF, in particular the functional Val66Met polymorphism (rs6265), have been found to be associated with a number of psychiatric disorders, cognitive function and obesity. As BDNF has been found to be differentially expressed in a number of aspects related to migraine, we tested for association between single nucleotide polymorphisms (SNPs) in BDNF and migraine. Methods. Five SNPs in the BDNF locus (rs1519480, rs6265, rs712507, rs2049046 and rs12273363) were genotyped initially in a cohort of 277 migraine cases, including 172 diagnosed with migraine with aura (MA) and 105 with migraine without aura (MO), and 277 age- and sex-matched controls. Three of these SNPs (rs6265, rs2049046 and rs12273363) were subsequently genotyped in a second cohort of 580 migraineurs, including 473 diagnosed with MA and 105 with O, and 580 matched controls. Results. – BDNF SNPs rs1519480, rs6265, rs712507 and rs12273363 were not significantly associated with migraine. However, rs2049046 showed a significant association with migraine, and in particular, MA in the first cohort. In the second cohort, although an increase in the rs2049046 T-allele frequency was observed in migraine cases, and in both MA and MO subgroups, it was not significantly different from controls. Analysis of data combined from both cohorts for rs2049046 showed significant differences in the genotypic and allelic distributions for this marker in both migraine and the MA sub-group. Conclusion. This study confirmed previous studies that the functional BDNF SNP rs6265 (Val66Met) is not associated with migraine. However, we found that rs2049046, which resides at the 5’ end of 3 one the BDNF transcripts, may be associated with migraine, suggesting that further investigations of this SNP may be warranted.

Ghrelin and the brain-gut axis as a pharmacological target for appetite control

Appetite regulation is highly complex and involves a large number of orexigenic and anorexigenic peptide hormones. These are small, processed, secreted peptides derived from larger prepropeptide precursors. These peptides are important targets for the development of therapeutics for obesity, a global health epidemic. As a case study, we consider the ghrelin axis. The ghrelin axis is likely to be a particularly useful drug target, as it also plays a role in energy homeostasis, adipogenesis, insulin regulation and reward associated with food intake. Ghrelin is the only known circulating gut orexigenic peptide hormone. As it appears to play a role in diet-induced obesity, blocking the action of ghrelin is likely to be effective for treating and preventing obesity. The ghrelin peptide has been targeted using a number of approaches, with ghrelin mirror-image oligonucleotides (Spiegelmers) and immunotherapy showing some promise. The ghrelin receptor, the growth hormone secretagogue receptor, may also provide a useful target and a number of antagonists and inverse agonists have been developed. A particularly promising new target is the enzyme which octanoylates ghrelin, ghrelin O-acyltransferase (GOAT), and drugs that inhibit GOAT are likely to circumvent pharmacological issues associated with approaches that directly target ghrelin or its receptor.

Understanding the abnormal brain activity in epilepsy as a potential predictor of the onset of an epileptic seizure

The Brain Research Institute (BRI) uses various types of indirect measurements, including EEG and fMRI, to understand and assess brain activity and function. As well as the recovery of generic information about brain function, research also focuses on the utilisation of such data and understanding to study the initiation, dynamics, spread and suppression of epileptic seizures. To assist with the future focussing of this aspect of their research, the BRI asked the MISG 2010 participants to examine how the available EEG and fMRI data and current knowledge about epilepsy should be analysed and interpreted to yield an enhanced understanding about brain activity occurring before, at commencement of, during, and after a seizure. Though the deliberations of the study group were wide ranging in terms of the related matters considered and discussed, considerable progress was made with the following three aspects. (1) The science behind brain activity investigations depends crucially on the quality of the analysis and interpretation of, as well as the recovery of information from, EEG and fMRI measurements. A number of specific methodologies were discussed and formalised, including independent component analysis, principal component analysis, profile monitoring and change point analysis (hidden Markov modelling, time series analysis, discontinuity identification). (2) Even though EEG measurements accurately and very sensitively record the onset of an epileptic event or seizure, they are, from the perspective of understanding the internal initiation and localisation, of limited utility. They only record neuronal activity in the cortical (surface layer) neurons of the brain, which is a direct reflection of the type of electrical activity they have been designed to record. 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Systematic differences in membrane acyl composition associated with varying body mass in mammals occur in all phospholipid classes : an analysis of kidney and brain

The acyl composition of membrane phospholipids in kidney and brain of mammals of different body mass was examined. It was hypothesized that reduction in unsaturation index (number of double bonds per 100 acyl chains) of membrane phospholipids with increasing body mass in mammals would be made-up of similar changes in acyl composition across all phospholipid classes and that phospholipid class distribution would be regulated and similar in the same tissues of the different-sized mammals. The results of this study supported both hypotheses. Differences in membrane phospholipid acyl composition (i. e. decreased omega-3 fats, increased monounsaturated fats and decreased unsaturation index with increasing body size) were not restricted to any specific phospholipid molecule or to any specific phospholipid class but were observed in all phospholipid classes. With increase in body mass of mammals both monounsaturates and use of less unsaturated polyunsaturates increases at the expense of the long-chain highly unsaturated omega-3 and omega-6 polyunsaturates, producing decreases in membrane unsaturation. The distribution of membrane phospholipid classes was essentially the same in the different-sized mammals with phosphatidylcholine (PC) and phosphatidylethanolamine (PE) together constituting similar to 91% and similar to 88% of all phospholipids in kidney and brain, respectively. The lack of sphingomyelin in the mouse tissues and higher levels in larger mammals suggests an increased presence of membrane lipid rafts in larger mammals. The results of this study support the proposal that the physical properties of membranes are likely to be involved in changing metabolic rate.