Brain image clustering by wavelet energy and CBSSO optimization algorithm

Previously, the diagnosis of brain abnormality was significantly important in the saving of social and hospital resources. Wavelet energy is known as an effective feature detection which has great efficiency in different utilities. This paper suggests a new method based on wavelet energy to automatically classify magnetic resonance imaging (MRI) brain images into two groups (normal and abnormal), utilizing support vector machine (SVM) classification based on chaotic binary shark smell optimization (CBSSO) to optimize the SVM weights. The results of the suggested CBSSO-based KSVM are compared favorably to several other methods in terms of better sensitivity and authenticity. The proposed CAD system can additionally be utilized to categorize the images with various pathological conditions, types, and illness modes

Soluble pre-fibrillar tau and β-amyloid species emerge in early human Alzheimer’s disease and track disease progression and cognitive decline

Acknowledgments We would like to gratefully acknowledge all donors and their families for the tissue provided for this study. Human tissue samples were supplied by the Brains for Dementia Research programme, jointly funded by Alzheimer’s Research UK, the Alzheimer’s Society and the Medical Research Council, and sourced from the MRC London Neurodegenerative Diseases Brain Bank, the Manchester Brain Bank, the South West Dementia Brain Bank (SWDBB), the Newcastle Brain Tissue Resource and the Oxford Brain Bank. The Newcastle Brain Tissue Resource and Oxford Brain Bank are also supported by the National Institute for Health Research (NIHR) Units. The South West Dementia Brain Bank (SWDBB) receives additional support from BRACE (Bristol Research into Alzheimer’s and Care of the Elderly). Alz-50, CP13, MC-1 and PHF-1 antibodies were gifted from Dr. Peter Davies and brain lystates from BACE1−/−mice were obtained from Prof Mike Ashford. The work presented here was funded by Alzheimer’s Research UK (Grant refs: ARUKPPG2014A-21 and ARUK-NSG2015-1 to BP and DK and NIH/NIA grants NIH/NINDS R01 NS082730 and R01 AG044372 to NK)Peer reviewedPublisher PD

Slowly expanding/evolving lesions as a magnetic resonance imaging marker of chronic active multiple sclerosis lesions.

BACKGROUND:Chronic lesion activity driven by smoldering inflammation is a pathological hallmark of progressive forms of multiple sclerosis (MS). OBJECTIVE:To develop a method for automatic detection of slowly expanding/evolving lesions (SELs) on conventional brain magnetic resonance imaging (MRI) and characterize such SELs in primary progressive MS (PPMS) and relapsing MS (RMS) populations. METHODS:We defined SELs as contiguous regions of existing T2 lesions showing local expansion assessed by the Jacobian determinant of the deformation between reference and follow-up scans. SEL candidates were assigned a heuristic score based on concentricity and constancy of change in T2- and T1-weighted MRIs. SELs were examined in 1334 RMS patients and 555 PPMS patients. RESULTS:Compared with RMS patients, PPMS patients had higher numbers of SELs (p = 0.002) and higher T2 volumes of SELs (p < 0.001). SELs were devoid of gadolinium enhancement. Compared with areas of T2 lesions not classified as SEL, SELs had significantly lower T1 intensity at baseline and larger decrease in T1 intensity over time. CONCLUSION:We suggest that SELs reflect chronic tissue loss in the absence of ongoing acute inflammation. SELs may represent a conventional brain MRI correlate of chronic active MS lesions and a candidate biomarker for smoldering inflammation in MS

The guilty brain: the utility of neuroimaging and neurostimulation studies in forensic field

Several studies have aimed to address the natural inability of humankind to detect deception and accurately discriminate lying from truth in the legal context. To date, it has been well established that telling a lie is a complex mental activity. During deception, many functions of higher cognition are involved: the decision to lie, withholding the truth, fabricating the lie, monitoring whether the receiver believes the lie, and, if necessary, adjusting the fabricated story and maintaining a consistent lie. In the previous 15 years, increasing interest in the neuroscience of deception has resulted in new possibilities to investigate and interfere with the ability to lie directly from the brain. Cognitive psychology, as well as neuroimaging and neurostimulation studies, are increasing the possibility that neuroscience will be useful for lie detection. This paper discusses the scientific validity of the literature on neuroimaging and neurostimulation regarding lie detection to understand whether scientific findings in this field have a role in the forensic setting. We considered how lie detection technology may contribute to addressing the detection of deception in the courtroom and discussed the conditions and limits in which these techniques reliably distinguish whether an individual is lying

What Makes Delusions Pathological?

Bortolotti argues that we cannot distinguish delusions from other irrational beliefs in virtue of their epistemic features alone. Although her arguments are convincing, her analysis leaves an important question unanswered: What makes delusions pathological? In this paper I set out to answer this question by arguing that the pathological character of delusions arises from an executive dysfunction in a subject’s ability to detect relevance in the environment. I further suggest that this dysfunction derives from an underlying emotional imbalance—one that leads delusional subjects to regard some contextual elements as deeply puzzling or highly significant

Nodes, paranodes and neuropathies

This review summarises recent evidence supporting the involvement of the specialised nodal and perinodal domains (the paranode and juxtaparanode) of myelinated axons in the pathology of acquired, inflammatory, peripheral neuropathies.The identification of new target antigens in the inflammatory neuropathies heralds a revolution in diagnosis, and has already begun to inform increasingly targeted and individualised therapies. Rapid progress in our basic understanding of the highly specialised nodal regions of peripheral nerves serves to strengthen the links between their unique microstructural identities, functions and pathologies. In this context, the detection of autoantibodies directed against nodal and perinodal targets is likely to be of increasing clinical importance. Antiganglioside antibodies have long been used in clinical practice as diagnostic serum biomarkers, and associate with specific clinical variants but not to the common forms of either acute or chronic demyelinating autoimmune neuropathy. It is now apparent that antibodies directed against several region-specific cell adhesion molecules, including neurofascin, contactin and contactin-associated protein, can be linked to phenotypically distinct peripheral neuropathies. Importantly, the immunological characteristics of these antibodies facilitate the prediction of treatment responsiveness

Cryptococcus, Pathological observations of five autopsy cases and one biopsy case

Pathologic, anatomical, and histological findings of 5 autopsy cases and one biopsy case of cryptococcosis have been described. Macroscopically the foci of the lung are grayish white or yellowish white in color and range in size from the small acinous-nodular ones to the larger lobular-nodular ones. In the brain the meninx appears gelatinous and edematous showing many small spots with indistinct boundary and with grayish white color. Lymph nodes infected with fungi are swollen in various degrees. Histologically the foci are mainly consisted of granulomatous inflammation containing giant cells. Besides, there are small degenerative foci having no inflammatory response and the lesions of marked fibrosis; the former will be newly formed foci and the latter the old ones. The size of C. neoformans found in tissue ranges from 3 to 30 &#956;, and the majority of fungi possess thick gelatinous capsule, but some of them in granulative lesions often possess no capsule. From the staining properties the capsule of C. neoformans is believed to be a kind of acid mucopolysaccharide. As for the staining method including general fungi, GOMORI's methenamine silver method is best, especially for the detailed examination of fungus structures, and for the differential diagnosis mucicarmine stain is the most suitable one. In tracing the distribution of the foci in the various organs, it seems that the first attack of this fungus occurs in the lung. The authors have called general attention, through their own experiences, to the fact that the small granulomatous foci caused by Cryptococcus infection, especially in the lung, may often escape the detection at autopsy.</p