Fruitless endeavor

There has been a small storm brewing lately about an exhibit of photographs that has been placed in the union. A minority of the pictures in the exhibit have pictures of naked bodies, specifically, naked women. These particular photographs have some members of the university community up in arms

Localizing unique and overlapping lesion locations in apraxia of speech and aphasia

Since Darley’s original description of apraxia of speech (AOS; 1968), controversy has centered around its diagnosis, treatment, and lesion location. Behaviors common to AOS are often shared among other communication disorders, complicating clinical management. The current study sought to identify crucial brain damage that causes apraxic speech, as well as errors common in both AOS and aphasia. Results revealed that damage to premotor and supplementary motor areas is unique to AOS, while involvement of temporal lobe areas predicts behaviors attributable to aphasia. These findings contribute to research regarding the neuroanatomical mechanism of AOS, and may ultimately improve differential diagnostic procedures

Localizing lesion locations to predict extent of aphasia recovery

Extensive research has related specific lesion locations to language impairment in aphasia. However, far less work has focused on the patterns of brain damage that predict prognosis in aphasia. The current study examined brain damage as a predictor of language recovery in acute patients with aphasia caused by stroke. Damage to the left posterior middle temporal gyrus (MTG) and left pars triangularis predicted poor recovery of speech production and MTG damage predicted less recovery of speech comprehension. These findings suggest that brain changes associated with language recovery rely on preservation and recruitment of the aforementioned areas in the left hemisphere

Allocentric neglect strongly associated with egocentric neglect.

To access publisher's full text version of this article. Please click on the hyperlink in Additional Links field.Following brain injury, many patients experience egocentric spatial neglect, where they fail to respond to stimuli on the contralesional side of their body. On the other hand, allocentric, object-based neglect refers to the symptom of ignoring the contralesional side of objects, regardless of the objects' egocentric position. There is an established tradition for considering these two phenomena as both behaviorally and anatomically dissociable. However, several studies and some theoretical work have suggested that these rather reflect two aspects of a unitary underlying disorder. Furthermore, in a recent large study Yue et al. [Archives of Physical Medicine and Rehabilitation 93 (2012) 156] reported that acute allocentric neglect is only observed in cases where substantial egocentric neglect is also present. In a new sample of right hemisphere stroke patients, we attempted to control for potential confounds by using a novel continuous measure for allocentric neglect (in addition to a recently developed continuous measure for egocentric neglect). Our findings suggest a strong association between egocentric and allocentric neglect. Consistent with the work of Yue et al. (2012), we found allocentric behavioral deficits only in conjunction with egocentric deficits as well as a large corresponding overlap for the anatomical regions associated with egocentric and with allocentric neglect. We discuss how different anatomical and behavioral findings can be explained in a unified physiologically plausible framework, whereby allocentric and egocentric effects interact.National Institutes of Health NS054266 DC009571 Deutsche Forschungsgemeinschaft KA 1258/10-1 HA 5839/3-1 PAK 270/

A model for the postcollapse equilibrium of cosmological structure: truncated isothermal spheres from top-hat density perturbations

The postcollapse structure of objects which form by gravitational condensation out of the expanding cosmological background universe is a key element in the theory of galaxy formation. Towards this end, we have reconsidered the outcome of the nonlinear growth of a uniform, spherical density perturbation in an unperturbed background universe - the cosmological ``top-hat'' problem. We adopt the usual assumption that the collapse to infinite density at a finite time predicted by the top-hat solution is interrupted by a rapid virialization caused by the growth of small-scale inhomogeneities in the initial perturbation. We replace the standard description of the postcollapse object as a uniform sphere in virial equilibrium by a more self-consistent one as a truncated, nonsingular, isothermal sphere in virial and hydrostatic equilibrium, including for the first time a proper treatment of the finite-pressure boundary condition on the sphere. The results differ significantly from both the uniform sphere and the singular isothermal sphere approximations for the postcollapse objects. These results will have a significant effect on a wide range of applications of the Press-Schechter and other semi-analytical models to cosmology. The truncated isothermal sphere solution presented here predicts the virial temperature and integrated mass distribution of the X-ray clusters formed in the CDM model as found by detailed, 3D, numerical gas and N-body dynamical simulations remarkably well. This solution allows us to derive analytically the numerically-calibrated mass-temperature and radius-temperature scaling laws for X-ray clusters which were derived empirically by Evrard, Metzler and Navarro from simulation results for the CDM model. (Shortened)Comment: 29 pages, 7 ps figures, MNRAS-style, LaTeX. Accepted for publication in MNRAS. Minor revisions only (including additional panel in Fig.3 and additional comparison with X-ray cluster simulations

Accumulation of Succinyl Coenzyme A Perturbs the Methicillin-Resistant Staphylococcus aureus (MRSA) Succinylome and Is Associated with Increased Susceptibility to Beta-Lactam Antibiotics

Penicillin binding protein 2a (PBP2a)-dependent resistance to β-lactam antibiotics in methicillin-resistant Staphylococcus aureus (MRSA) is regulated by the activity of the tricarboxylic acid (TCA) cycle via a poorly understood mechanism. We report that mutations in sucC and sucD, but not other TCA cycle enzymes, negatively impact β-lactam resistance without changing PBP2a expression. Increased intracellular levels of succinyl coenzyme A (succinyl-CoA) in the sucC mutant significantly perturbed lysine succinylation in the MRSA proteome. Suppressor mutations in sucA or sucB, responsible for succinyl-CoA biosynthesis, reversed sucC mutant phenotypes. The major autolysin (Atl) was the most succinylated protein in the proteome, and increased Atl succinylation in the sucC mutant was associated with loss of autolytic activity. Although PBP2a and PBP2 were also among the most succinylated proteins in the MRSA proteome, peptidoglycan architecture and cross-linking were unchanged in the sucC mutant. These data reveal that perturbation of the MRSA succinylome impacts two interconnected cell wall phenotypes, leading to repression of autolytic activity and increased susceptibility to β-lactam antibiotics. IMPORTANCE mecA-dependent methicillin resistance in MRSA is subject to regulation by numerous accessory factors involved in cell wall biosynthesis, nucleotide signaling, and central metabolism. Here, we report that mutations in the TCA cycle gene, sucC, increased susceptibility to β-lactam antibiotics and was accompanied by significant accumulation of succinyl-CoA, which in turn perturbed lysine succinylation in the proteome. Although cell wall structure and cross-linking were unchanged, significantly increased succinylation of the major autolysin Atl, which was the most succinylated protein in the proteome, was accompanied by near complete repression of autolytic activity. These findings link central metabolism and levels of succinyl-CoA to the regulation of β-lactam antibiotic resistance in MRSA through succinylome-mediated control of two interlinked cell wall phenotypes. Drug-mediated interference of the SucCD-controlled succinylome may help overcome β-lactam resistance

Not on the edge: the syntax and pragmatics of clause-initial negation in Swedish

The possibility of topicalizing sentential negation is severely restricted in the Germanic V2-languages. In this paper, we show that negative preposing was more frequent and less restricted in earlier stages of Swedish: approx. 8 % of all occurrences of negation are clause initial in Old Swedish, compared to less than 0.5 % in present day Swedish. We propose that this change in frequency can be traced to the syntactic status of the negative element. More specifically, we argue that Old Swedish eigh 'not' may function as a syntactic head and cliticize to the finite verb in [C-0]. This possibility is not open to the XP inte 'not' in Modern Swedish. In Modern Swedish, we argue that the restrictions on negative preposing instead are related to more general pragmatic restrictions on the information expressed in [Spec,CP]: according to our hypothesis, negative preposing is licensed by contrast

Understanding within-session loss-chasing: an experimental investigation of the impact of stake size on cognitive control

Loss-chasing is a central feature of problematic gambling, yet it remains a poorly conceived and understood concept. Loss-chasing is believed to stem from an ero- sion of cognitive control when gambling. The opportunity to gamble at significantly dis- parate stake sizes on a gambling activity is considered to be a risk factor for loss-chasing. This study investigated the impact of gambling at disparate stake sizes on executive processes integral to maintaining cognitive control when gambling, namely response inhibition and reflection impulsivity. Frequent adult non-problem gamblers (n = 32) participated in a repeated measures experiment; and gambled at three disparate stake sizes (£20, £2 and no stake per bet) on a simulated gambling task. Participants’ response inhibition performance and reflection impulsivity levels after gambling at various stake sizes were compared via a go/no-go task and information sampling task, respectively. Quality of decision-making i.e. the evaluation of available information to make probability judgements was impaired after gambling at higher stakes in comparison to lower stakes, indicating an increase in reflection impulsivity. No effect on response inhibition was observed. Although exploratory, this suggests that the opportunity for participants to substantially increase stake size on a gambling activity may be a risk factor for impaired cognitive performance when gambling, and perhaps create vulnerability for within-session loss-chasing in some players. Keywords Problem gambling - Cognitive control - Loss-chasing - Response inhibition - Reflection impulsivit

Ethanol and Cognition: Indirect Effects, Neurotoxicity and Neuroprotection: A Review

Ethanol affects cognition in a number of ways. Indirect effects include intoxication, withdrawal, brain trauma, central nervous system infection, hypoglycemia, hepatic failure, and Marchiafava-Bignami disease. Nutritional deficiency can cause pellagra and Wernicke-Korsakoff disorder. Additionally, ethanol is a direct neurotoxin and in sufficient dosage can cause lasting dementia. However, ethanol also has neuroprotectant properties and in low-to-moderate dosage reduces the risk of dementia, including Alzheimer type. In fetuses ethanol is teratogenic, and whether there exists a safe dose during pregnancy is uncertain and controversial