Post-stroke dementia (PSD) or post-stroke cognitive impairment (PSCI) may affect up to one third of stroke survivors. Various definitions of PSCI and PSD have been described. We propose PSD as a label for any dementia following stroke in temporal relation. Various tools are available to screen and assess cognition, with few PSD-specific instruments. Choice will depend on purpose of assessment, with differing instruments needed for brief screening (e.g., Montreal Cognitive Assessment) or diagnostic formulation (e.g., NINDS VCI battery). A comprehensive evaluation should include assessment of pre-stroke cognition (e.g., using Informant Questionnaire for Cognitive Decline in the Elderly), mood (e.g., using Hospital Anxiety and Depression Scale), and functional consequences of cognitive impairments (e.g., using modified Rankin Scale). A large number of biomarkers for PSD, including indicators for genetic polymorphisms, biomarkers in the cerebrospinal fluid and in the serum, inflammatory mediators, and peripheral microRNA profiles have been proposed. Currently, no specific biomarkers have been proven to robustly discriminate vulnerable patients (‘at risk brains’) from those with better prognosis or to discriminate Alzheimer’s disease dementia from PSD. Further, neuroimaging is an important diagnostic tool in PSD. The role of computerized tomography is limited to demonstrating type and location of the underlying primary lesion and indicating atrophy and severe white matter changes. Magnetic resonance imaging is the key neuroimaging modality and has high sensitivity and specificity for detecting pathological changes, including small vessel disease. Advanced multi-modal imaging includes diffusion tensor imaging for fiber tracking, by which changes in networks can be detected. Quantitative imaging of cerebral blood flow and metabolism by positron emission tomography can differentiate between vascular dementia and degenerative dementia and show the interaction between vascular and metabolic changes. Additionally, inflammatory changes after ischemia in the brain can be detected, which may play a role together with amyloid deposition in the development of PSD. Prevention of PSD can be achieved by prevention of stroke. As treatment strategies to inhibit the development and mitigate the course of PSD, lowering of blood pressure, statins, neuroprotective drugs, and anti-inflammatory agents have all been studied without convincing evidence of efficacy. Lifestyle interventions, physical activity, and cognitive training have been recently tested, but large controlled trials are still missing.

Functional magnetic resonance imaging (fMRI) was used to determine whether visual responses to food in the human amygdala and related corticolimbic structures would be selectively altered by changes in states of hunger. Participants viewed images of motivationally relevant (food) and motivationally irrelevant (tool) objects while undergoing fMRI in alternately hungry and satiated conditions. Food-related visual stimuli elicited greater responses in the amygdala, parahippocampal gyrus. and anterior fusiform gyrus when participants were in a hungry state relative to a satiated state. The state-dependent activation of these brain structures did not generalize to the motivationally irrelevant objects. These results support the hypothesis that the amygdala and associated inferotemporal regions are involved in the integration of subjective interoceptive states with relevant sensory cues processed along the ventral visual stream.

No abstract

Highlights d The SLC1A5 variant is a mitochondrial glutamine transporter d The SLC1A5 variant has a mitochondrial targeting sequence d Hypoxia controls SLC1A5 variant expression through HIF-2a d The SLC1A5 variant mediates mitochondrial glutamine metabolism in cancer

Functional MRI was used to examine cerebral activations in 12 subjects while they performed a spatial attention task. This study applied more stringent behavioural and cognitive controls than previously used for similar experiments: (i) subjects were included only if they showed evidence of attentional shifts while performing the task in the magnet; (ii) the experimental task and baseline condition were designed to eliminate the contributions of motor output, visual fixation, inhibition of eye movements, working memory and the conditional (no-go) component of responding. Activations were seen in all three hypothesized cortical epicentres forming a network for spatial attention: the lateral premotor cortex (frontal eye fields), the posterior parietal cortex and the cingulate cortex. Subcortical activations were seen in the basal ganglia and the thalamus. Although the task required attention to be equally shifted to the left and to the right, eight of 10 subjects showed a greater area of activation in the right parietal cortex, consistent with the specialization of the right hemisphere for spatial attention. Other areas of significant activation included the posterior temporo-occipital cortex and the anterior insula. The temporo-occipital activation was within a region broadly defined as MT+ (where MT is the middle temporal area) which contains the human equivalent of area MT in the macaque monkey. This temporo-occipital area appears to constitute a major component of the functional network activated by this spatial attention task. Its activation may reflect the 'inferred' shift of the attentional focus across the visual scene.

IntroductionPostnatal tissue neovascularization is an important adaptation for rescue from critical ischemia and is required for sufficient blood supply to growing tumors. This process was formerly attributed to the migration and proliferation of pre-existing, fully differentiated endothelial cells (ECs) in a process called angiogenesis. Recent studies have shown that circulating bone marrow (BM)-derived endothelial progenitor cells (EPCs) are recruited to the site of tissue regeneration and substantially contribute to neovascularization and re-endothelialization after acute vascular injury. 1,2 Intravenous infusion of EPCs after ischemia was shown to improve neovascularization and cardiac function in both animal models and pilot clinical studies. Conversely, BM-derived EPCs participate in the pathogenesis of various diseases, such as cancer, retinopathy, and atherosclerosis. 2,3 Impaired recruitment of BM-derived endothelial and hematopoietic precursor cells is known to block both tumor angiogenesis and growth. 4 Injection of BM cells promotes injuryassociated retinal angiogenesis. 5 BM-derived progenitors also contribute to the formation of the microvasculature in allograft arteriosclerotic lesions. 6 Therefore, EPCs have both physiologic and pathologic roles; thus, they have been widely considered for establishing new therapeutic strategies for the treatment of angiogenesis-related diseases.The number of circulating EPCs may limit the ultimate magnitude of angiogenesis therapies and, therefore, strategies that are based on the administration of ex vivo-expanded populations of EPCs harvested from the patient's circulating blood appear promising. 7 In addition, increased recruitment and specific lodging of EPCs in ischemic tissues may constitute another therapeutic target. Likewise, mechanisms to prevent EPC homing show promise as therapeutic strategies for the treatment of excessive neovascularization. Recently, stromal cell-derived factor-1 (SDF-1), a member of the chemokine CXC subfamily, was identified as an important factor for the trafficking of EPCs to ischemic tissues; it has also been recognized as a prominent target for increasing the engraftment of progenitor cells. 8,9 SDF-1 secreted from carcinomaassociated fibroblasts promotes angiogenesis by recruiting EPCs to tumor tissue. 3 Furthermore, ␤2-integrin expressed in EPCs was shown to mediate augmentation of the homing and neovascularization capacity of EPCs in vitro and in vivo. 10 CXCR2 also increased the homing of circulating EPCs to the sites of artery injury, possibly by enhancing adhesion of EPCs to extracellular matrix coimmobilized with chemokines. 11,12 Therefore, the identification of novel, endogenous factors that lead to both the mobilization and homing of EPCs in response to tissue hypoxia is important for the understanding of the functional contribution of EPCs to postnatal neovascularization and to the establishment of new strategies for the treatment of angiogenesis-related diseases. Here, we report a novel role and underlying signali...

BackgroundThe purpose of present study was to examine biological and psychological characteristics of people according to the Sasang typology, which is popular in Korea. We evaluated the Sasang Personality Questionnaire (SPQ) as a measure of temperament, and Body Mass Index (BMI) as a measure of the somatic properties of each Sasang type.MethodsSubjects were 2506 (877 males, 1629 females) outpatients between the ages of 20 through 70 who requested traditional medical assessment and treatment in Korea. The structural validity of the SPQ was examined and its correlation with BMI was analyzed. The SPQ and BMI measures of each Sasang type across age and gender were presented and their differences were analyzed with Analysis of Variance.ResultsConfirmatory factor analysis and path analysis identified an acceptable three-factor structure of the SPQ measuring differences in individual’s behavior, emotion, and cognition. SPQ scores (29.71 ± 1.00, 28.29 ± 0.19 and 26.14 ± 0.22) and BMI scores (22.92 ± 0.09, 25.56 ± 0.10 and 21.44 ± 0.10) were significantly (p < 0.001) different among So-Yang, Tae-Eum and So-Eum Sasang types, respectively.ConclusionsThe results showed that the SPQ and BMI is a reliable measure for quantifying the biopsychological characteristics of each types, and useful for guiding personalized and type-specific treatment with medical herbs and acupuncture.

No abstract