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Abstract During domestication animals have undergone changes in size of brain and other vital organs. We hypothesize that this could be a correlated effect to increased tameness. Red Junglefowl (ancestors of domestic chickens) were selected for divergent levels of fear of humans for five generations. The parental (P0) and the fifth selected generation (S5) were culled when 48–54 weeks old and the brains were weighed before being divided into telencephalon, cerebellum, mid brain and optic lobes. Each single brain part as well as the liver, spleen, heart and testicles were also weighed. Brains of S5 birds with high fear scores (S5 high) were heavier both in absolute terms and when corrected for body weight. The relative weight of telencephalon (% of brain weight) was significantly higher in S5 high and relative weight of cerebellum was lower. Heart, liver, testes and spleen were all relatively heavier (% of body weight) in S5 high. Hence, selection for tameness has changed the size of the brain and other vital organs in this population and may have driven the domesticated phenotype as a correlated response.

To develop a potential SPECT probe to evaluate the integrity of the serotoninergic system (5-HTT) whose dysfunction is linked to several disease conditions such as Parkinson's disease, Alzheimer's disease and depression, we report the synthesis, radiolabeling and in vivo baboon imaging of 2beta-carbomethoxy-3beta-(3'-[(123)I]iodophenyl) tropane (YP256, 6). The radiolabeling was performed by iododestannylation using sodium [(123)I]iodide and peracetic acid. Although the ligand displayed high selectivity for 5-HTT over dopamine transporter in vitro, SPECT imaging in baboons did not reveal selective 5-HTT accumulation in brain in vivo.

What is rotated in mental rotation? The implicitly or explicitly most widely accepted assumption is that the rotated representation is a visual mental image. We here provide converging evidence that instead mental rotation is a process specialized on a certain type of spatial information. As a basis, we here develop a general theory on how to manipulate and empirically examine representational content. One technique to examine the content of the representation in mental rotation is to measure the influence of stimulus characteristics on rotational speed. Experiment 1a and 1b show that the rotational speed of university students (10 men, 10 women and 10 men, 11 women, respectively) is influenced exclusively by the amount of represented orientation-dependent spatial-relational information but not by orientation-independent spatial-relational information, visual complexity, or the number of stimulus parts. Obviously, only explicit orientation-dependent spatial-relational information in an abstract, nonvisual form is rotated. As information in mental-rotation tasks is initially presented visually, a nonvisual representation during rotation implies that at some point during processing information is recoded. Experiment 2 provides more direct evidence for this recoding. While university students (12 men, 12 women) performed our mental-rotation task, we recorded their EEG in order to extract slow potentials, which are sensitive to working-memory load. During initial stimulus processing, slow potentials were sensitive to the amount of orientation-independent information or to the visual complexity of the stimuli. During rotation, in contrast, slow potentials were sensitive to the amount of orientation-dependent information only. This change in slow potential behavior constitutes evidence for the hypothesized recoding of the content of the mental representation from a visual into a nonvisual form. We further assumed that, in order to be accessible for the process of mental rotation, orientation-dependent information must be represented in those brain areas that are also responsible for mental rotation proper. Indeed, in an fMRI study on university students (12 men, 12 women) the very same set of brain areas was specifically activated by both the amount of mental rotation and of orientation-dependent information. The amount of orientation-independent information/visual complexity, in contrast, influenced activation in a different set of brain areas. Together, all activated areas constitute the so-called mental rotation network. In sum, the present work provides a general theory and several techniques to examine mental representations and employs these techniques to identify the content, timing, and neuronal source of the mental representation in mental rotation. Was wird bei mentaler Rotation rotiert? Die implizit oder explizit am weitesten verbreitete Annahme ist, dass die rotierte Repräsentation ein mentales Bild ist. Wir berichten hier konvergierende Evidenz, dass mentale Rotation stattdessen ein auf einen bestimmten Typ räumlicher Information spezialisierter Prozess ist. Als Grundlage entwickeln wir hier zunächst eine allgemeine Theorie, wie der Inhalt einer Repräsentation manipuliert und empirisch untersucht werden kann. Eine Technik, den Inhalt der Repräsentation bei mentaler Rotation zu untersuchen, ist den Einfluss von Stimuluseigenschaften auf die Rotationsgeschwindigkeit zu messen. Experiment 1a und 1b zeigen, dass die Rotationsgeschwindigkeit von Studenten (10 Männer, 10 Frauen bzw. 10 Männer, 11 Frauen) ausschließlich von der Menge an repräsentierter orientierungsabhängiger räumlich-relationaler Information, aber nicht von orientierungsunabhängiger räumlich-relationaler Information, visueller Komplexität oder der Anzahl an Stimulusteilen beeinflusst wird. Offensichtlich wird nur explizite orientierungsabhängige räumlich-relationale Information in einer abstrakten, nicht-visuellen Form rotiert. Da Informationen in Experimenten zur mentalen Rotation ursprünglich visuell präsentiert werden, impliziert eine nicht-visuelle Repräsentation während der Rotation, dass, zu einem gewissen Punkt während der Verarbeitung, Informationen umkodiert werden. Experiment 2 liefert direktere Evidenz für diese Umkodierung: Während Studenten (12 Männer, 12 Frauen) an unserem Experiment zur mentalen Rotation teilnahmen, zeichneten wir ihr EEG auf, um langsame Potentiale zu extrahieren, welche sensitiv für Arbeitsgedächtnisbelastung sind. Zu Beginn der Stimulus-Verarbeitung waren diese langsamen Potentiale sensitiv für die Menge an orientierungsunabhängiger Information bzw. für die visuelle Komplexität der Stimuli. Im Gegensatz dazu waren die langsamen Potentiale während der Rotation ausschließlich sensitiv für die Menge an orientierungsabhängiger Information. Diese Veränderung der langsamen Potentiale stellt Evidenz für die postulierte Umkodierung des Inhalts der mentalen Repräsentation von einer visuellen in eine nicht-visuelle Form dar. Weiterhin nahmen wir an, dass, damit sie für den Prozess der mentalen Rotation zugänglich ist, orientierungsabhängige Information in den Hirnarealen repräsentiert sein muss, die auch für die mentale Rotation selbst zuständig sind. Tatsächlich war in einer fMRI-Studie mit Studenten (12 Männer, 12 Frauen) dasselbe Netz an Hirnarealen, das spezifisch durch die Menge an mentaler Rotation aktiviert war, auch spezifisch durch die Menge an orientierungsabhängiger Information aktiviert. Die Menge an orientierungsunabhängiger Information hingegen beeinflusste die Aktivation in einem anderen Netz an Hirnarealen. In ihrer Gesamtheit stellen alle aktivierten Areale das sogenannte Netzwerk der mentalen Rotation dar. Zusammengefasst liefert die vorliegende Arbeit eine allgemeine Theorie und mehrere Techniken zur Untersuchung von mentalen Repräsentationen und setzt diese Techniken ein, um den Inhalt, den zeitlichen Verlauf und den neuronalen Ursprung der mentalen Repräsentation bei mentaler Rotation zu untersuchen.

Abstract Background This work examines the central nervous system distribution of virus-labeled neurons from the rat urinary bladder and the prostate simultaneously within the same tissue sections. Two immunohistochemically distinct pseudorabies virus strains were simultaneously injected into male Sprague Dawley rats (~280 gm). One virus was injected into the bladder and the other into the prostate. After incubation intervals of 2.25, 2.5, 2.75, 3 and 4 days, sections from the spinal cord and brain were processed immunohistochemically to detect cells, within a single section, which were labeled separately by each virus or were labeled by both viruses. Results Each strain of virus labeled a separate population of neurons and some neurons were labeled by both strains. The majority of neurons labeled by virus from the urinary bladder were found in the L6-S1 spinal cord segments within the dorsal gray commissure, the intermediolateral area and the superficial dorsal horn. Neurons labeled by virus from the prostate were mainly found in the L1-L2 spinal cord segments in the dorsal gray commissure and the intermediolateral areas. Double-labeled interneurons in L1-L2 were mainly located in the intermediolateral area. In L6-S1 they were divided between the dorsal gray commissure and the intermediolateral area. Conclusions Spinal neurons innervating the bladder are clearly separate and different from those innervating the prostate. This difference also persists in the brain. In disagreement with previous reports, no direct anatomical evidence of parasympathetic innervation of the prostate was observed.

PURPOSE: To determine the significance of vascular enhancement in stroke patients with and without permanent neurologic deficit. METHODS: We prospectively studied two groups of patients with spin-echo MR imaging before and after injection of gadopentetate dimeglumine. In the patients in group 1 (12 women, 22 men; age range, 32 to 76 years), who had permanent neurologic deficit caused by recent ischemic brain infarction, we obtained 3 to 13 serial MR images during follow-up examination. Group 2 consisted of 26 patients (14 women, 12 men; age range, 54 to 81 years) with transient neurologic deficit caused by angiographically proved high-grade stenosis or occlusion of the internal carotid artery. RESULTS: Vascular enhancement was present in 59% of patients in group 1 and in 65% of patients of group 2. In group 1, the frequency of vascular enhancement declined steadily over several weeks, but it was still present in single cases even after 3 months. Vascular enhancement correlated positively with the extent of brain infarction in group 1 and with the degree of carotid stenosis in group 2. CONCLUSION: Vascular enhancement as shown by MR imaging may herald ischemic brain infarction and could persist over several weeks in areas that show collateral flow after infarction has occurred.

OBJECTIVE: To review and synthesize the clinical literature regarding risks and benefits of omentum transplantation and transposition surgery in patients with ischemic stroke of other etiology (non-MMD) and Moyamoya disease (MMD), and to evaluate the evidence for biological underpinnings of the presumed physiologic effects of omentum transplantation and transposition on vascularization of brain parenchyma.METHODS: Articles were searched on scientific databases using predefined key terms. Data abstraction was based on the clinical course as reported in the articles. For further analysis, patients were divided into groups according to their diagnosis (MMD or non-MMD). Descriptive statistics were computed for better integration of the results.RESULTS: The final literature review contained 15 articles (11 case series, 4 single case studies) with data on 93 patients (29 non-MMD, 64 MMD). At post-assessment 56% of patients showed substantial gains in functional domains (24% in the non-MMD group, 71% in the MMD group) and 92% demonstrated improvements of cerebral vascularization (55% in the non-MMD group, 98% in the MMD group). Differences in improvement became apparent with regard to the initial symptomatology wherein transient ischemic attacks were related to superior recovery rates and language pathologies showed least improvement.CONCLUSIONS: Surgical revascularization using omental tissue has shown good success rates, particularly for recurrent transient ischemic attacks and prevention of further strokes and should be considered as treatment option for selected patients. Experimental data on the physiologic basis for postoperative improvement delivered convincing evidence for its arteriogenic potential and recent developments in omental stem cell research suggest a role in recovery from long-standing neurological deficits.

Anxiety and fear are evolutionarily conserved emotions that increase the likeli-hood of an organism surviving threatening situations. Anxiety and vigilance states are regulated by neural networks involving multiple brain regions. In anx-iety disorders, this intricate regulatory system is disturbed, leading to excessive or prolonged anxiety or fear. Anxiety disorders have both genetic and environ-mental risk factors. Genetic research has the potential to identify specific genetic variants causally associated with specific phenotypes. In recent decades, genome-wide association studies (GWASs) have revealed variants predisposing to neuropsychiatric disorders, suggesting novel neurobiological pathways in the etiology of these disorders. Here, we review recent human GWASs of anxiety dis -orders, and genetic studies of anxiety-like behavior in rodent models. These studies are paving the way for a better understanding of the neurobiological mechanisms underlying anxiety disorders. Peer reviewed

AI-based methods have shown great promise in a variety of biomedical research fields, including neurooncologic imaging. For example, machine learning methods have offered informative predictions of overall survival (OS) and progression-free survival (PFS), differentiation between pseudoprogression (PsP) and progressive disease (PD), and estimation of mutational status from imaging data. Despite their promise, AI, and especially the emerging deep learning (DL) methods, are challenged by several factors, including imaging heterogeneity across scanners and lack of sufficiently large and diverse training datasets, which limits their reproducibility and general acceptance. These challenges prompted the development of the ReSPOND (Radiomics Signatures for PrecisiON Diagnostics) consortium on glioblastoma, a growing effort to bring together a community of researchers sharing imaging, demographic, clinical and (currently) limited molecular data in order to address the following aims: 1) pool and harmonize data across diverse hospitals and patient populations worldwide; 2) derive robust and generalizable AI models for prediction of (initially) OS, PFS, PsP vs. PD, and recurrence; 3) test these predictive models across multiple sites. In its first phase, ReSPOND aims to pool together approximately 3,000MRI scans (from 10institutions plus TCIA), along with demographics, KPS, and (for a subset) MGMT/IDH1 status. We present initial results testing the generalization of a previously trained model of OS on 505Penn datasets to 2independent cohorts from Case Western Reserve University and University Hospitals (N=44), and Penn (N=67). The results indicate good generalization, with correlation coefficients between OS/predicted-OS between 0.25 to 0.5, depending on variable availability, which is comparable to cross-validated accuracy previously obtained from the training set itself (N=505). Additional preliminary studies evaluating prediction of future recurrence from baseline pre-operative scans in de novo patients (Penn model applied to CWR) indicated potential for guiding targeted dose escalation and supra-total resection (excellent predictions in 6/12 patients, modest in 1/12, and poor in 5/12).

Drug addiction is a state of altered brain reward and self-regulation mediated by both neurotransmitter and hormonal systems. Although an organism’s internal system attempts to maintain homeostasis when challenged by exogenous opiates and other drugs of abuse, it eventually fails, resulting in the transition from drug use to drug abuse. We propose that the attempted maintenance of hormonal homeostasis is achieved, in part, through alterations in levels of processing enzymes that control the ratio of active hormone to pro-hormone. Two pro-hormone convertases, PC1/3 and PC2 are believed to be responsible for the activation of many neurohormones and expression of these enzymes is dependent on the presence of a cyclic-AMP response element (CRE) in their promoters. Therefore, we studied the effects of short-term (24-h) and long-term (seven-day) morphine treatment on the expression of hypothalamic PC1/3 and PC2 and levels of phosphorylated cyclic-AMP-response element binding protein (P-CREB). While short-term morphine exposure down-regulated, long-term morphine exposure up-regulated P-CREB, PC1/3 and PC2 protein levels in the rat hypothalamus as determined by Western blot analysis. Quantitative immunofluorescence studies confirmed these regulatory actions of morphine in the paraventricular and dorsomedial nucleus of the hypothalamus. Specific radioimmunoassays demonstrated that the increase in PC1/3 and PC2 levels following long-term morphine led to increased TRH biosynthesis as evidence by increased TRH/5.4 kDa C-terminal proTRH-derived peptide ratios in the median eminence. Promoter activity experiments in rat sommatomammotrope GH3 cells containing the mu-opioid receptor demonstrated that the CRE(s) in the promoter of PC1/3 and PC2 is required for morphine-induced regulation of PC1/3 and PC2. Our data suggest that the regulation of the prohormone processing system by morphine may lead to alterations in the levels of multiple bioactive hormones and may be a compensatory mechanism whereby the organism tries to restore its homeostatic hormonal milieu. The down-regulation of PC1/3, PC2 and P-CREB by short-term morphine and up-regulation by long-term morphine treatment may be a signal mediating the switch from drug use to drug abuse.

AIM: To analyze the Glutathione S-transferase (GST)-P, GST-M, cytochrome p450 (CYP)1-A1, CYP1-B1, and multidrug resistance (MDR)-1 expressions in malignant intracranial tumor (ICT)s, and to elicit their role on patient survival. MATERIAL and METHODS: GST-P, GST-M, CYP1-A1, CYP1-B1, and MDR-1 expressions were analyzed using immunostaining in 149 samples from 141 patients with preoperative ICT diagnosis. The case characteristics were reviewed, and the enzyme expressions were equated based on the age, gender, and tumor type. Then, 77 of 141 patients with malignant ICT and complete medical records postoperative were also investigated in detail for the relationship between the diagnosis, enzyme expression, and overall survival. RESULTS: The average age was 49.44 years, with 83 (58.45%) male patients. Among the 77 malignant ICTs, 38 (49.3%) and 29 were glial tumors and metastases, respectively, with a 13.35-month overall survival. Patients with metastatic tumor have approximately threefold higher GSTP level than those with glial tumors. MDR-1 expression was approximately twofold higher in > 60-year-old patients. No statistically significant association was found between patients' smoking behaviors, alcohol consumption, and overall survival. Only MDR-1 expression was correlated with overall survival. Better overall survival was observed in patients with a negative MDR-1 expression than those with a positive one.