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Prelinguistic babbling is a critical phase in infant language development and is best understood in temperate songbirds where it occurs primarily in males at reproductive maturity and is modulated by sex steroids. Parrots of both sexes are icons of tropical vocal plasticity, but vocal babbling is unreported in this group and whether the endocrine system is involved is unknown. Here we show that vocal babbling is widespread in a wild parrot population in Venezuela, ensues in both sexes during the nestling stage, occurs amidst a captive audience of mixed-aged siblings, and is modulated by corticosteroids. Spectrographic analysis and machine learning found phoneme diversity and combinatorial capacity increased precipitously for the first week, thereafter, crystalizing into a smaller repertoire, consistent with the selective attrition model of language development. Corticosterone-treated nestlings differed from unmanipulated birds and sham controls in several acoustic properties and crystallized a larger repertoire post-treatment. Our findings indicate babbling occurs during an early life-history stage in which corticosteroids help catalyse the transition from a universal learning programme to one finely tuned for the prevailing ecological environment, a potentially convergent scenario in human prelinguistic development.

Abstract Background Sodium weighted images can indicate sodium signal intensities from different features in the tumor before and 24 hours following administration of Taxotere. Aim To evaluate the association of in vivo intracellular sodium magnetic resonance image intensities with immuno-biomarkers and histopathological features to monitor the early tumor response to Taxotere chemotherapy in Methyl-Nitroso-Urea induced rat xenograft breast tumors. Methods and Materials Methyl-Nitroso-Urea (MNU) induced rat xenograft breast tumors were imaged for sodium MRI and compared with tumor histology, immunostaining after 24 hours chemotherapy. Results Sodium MRI signal intensities represented sodium concentrations. Excised tumor histological sections showed different in vitro histological end points i.e. single strand DNA content of cell nuclei during cell cycle (G1/S-G2/M), distinct S or M histograms (Feulgen labeling to nuclear DNA content by CAS 200), mitotic figures and apoptosis at different locations of breast tumors. Necrosis and cystic fluid appeared gray on intracellular (IC) sodium images while apoptosis rich regions appeared brighter on IC sodium images. After 24 hours Taxotere-treated tumors showed lower 'IC/EC ratio' of viable cells (65–76%) with higher mitotic index; apoptotic tumor cells at high risk due to cytotoxicity (>70% with high apoptotic index); reduced proliferation index (270 vs 120 per high power field) associated with enhanced IC sodium in vivo MR image intensities and decreased tumor size (3%; p < 0.001; n = 16) than that of pre-treated tumors. IC-Na MR signal intensities possibly indicated Taxotere chemosensitivity response in vivo associated with apoptosis and different pre-malignant features within 24 hours of exposure of cancer cells to anti-neoplastic Taxotere drug. Conclusion Sodium MRI imaging may be used as in vivo rapid drug monitoring method to evaluate Taxotere chemosensitivity response associated with neoplasia, apoptosis and tumor histology features.

Abstract Flow cytometry, DNA fragmentation, ion ratiomateric analysis and NMR peaks characterized drug chemosensitivity of antineoplastic drugs. Hypotheses were: 1. The chemosensitive effect of different cancer cell lines is characteristic; 2. DNA fragmentation, ion ratiometric analysis suggest apoptosis status of tumor cells. Methods PC-3 cell lines were compared with DU-145, LNCaP cell lines in culture for the [Na]i and [Ca]i ion sensing dyes, cell death, NMR peaks and apoptosis staining for chemotherapeutic action of different drugs. Results DNA fragmentation, ratiometric ions and fluorescence endlabelling plots were characteristic for cell lines and drug response. 31P-23Na NMR spectra showed characteristic high phospho-choline and sodium peaks. Conclusion Flow cytometry, DNA fragmentation, ion ratiometric methods and NMR peaks indicated apoptosis and offered in vivo drug monitoring method.

The Alzheimer's Disease Neuroimaging (ADNI) database is an expansive undertaking by government, academia, and industry to pool resources and data on subjects at various stage of symptomatic severity due to Alzheimer's disease. As expected, magnetic resonance imaging is a major component of the project. Full brain images are obtained at every 6-month visit. A range of cognitive tests studying executive function and memory are employed less frequently. Two blood draws (baseline, 6 months) provide samples to measure concentrations of approximately 145 plasma biomarkers. In addition, other diagnostic measurements are performed including PET imaging, cerebral spinal fluid measurements of amyloid-beta and tau peptides, as well as genetic tests, demographics, and vital signs. ADNI data is available upon review of an application. There have been numerous reports of how various processes evolve during AD progression, including alterations in metabolic and neuroendocrine activity, cell survival, and cognitive behavior. Lacking an analytic model at the onset, we leveraged recent advances in machine learning, which allow us to deal with large, non-linear systems with many variables. Of particular note was examining how well binary predictions of future disease states could be learned from simple, non-invasive measurements like those dependent on blood samples. Such measurements make relatively little demands on the time and effort of medical staff or patient. We report findings with recall/precision/area under the receiver operator curve after application of CART, Random Forest, Gradient Boosting, and Support Vector Machines, Our results show (i) Random Forests and Gradient Boosting work very well with such data, (ii) Prediction quality when applied to relatively easily obtained measurements (Cognitive scores, Genetic Risk and plasma biomarkers) achieve results that are competitive with magnetic resonance techniques. This is by no means an exhaustive study, but instead an exploration of the plausibility of defining a series of relatively inexpensive, broad population based tests. [ABSTRACT FROM AUTHOR]

Pinsky, David J., Walif Aji, Matthias Szabolcs, Eleni S. Athan, Youping Liu, Yi Ming Yang, Richard P. Kline, Kim E. Olson, and Paul J. Cannon. Nitric oxide triggers programmed cell death (apoptosis) of adult rat ventricular myocytes in culture. Am. J. Physiol. 277 (Heart Circ. Physiol. 46): H1189-H1199, 1999.--Excessive nitric oxide (NO) production within the heart is implicated in the pathogenesis of myocyte death, but the mechanism whereby NO kills cardiac myocytes is not known. To determine whether NO may trigger programmed cell death (apoptosis) of adult rat ventricular myocytes in culture, the NO donor S-nitroso-N-acetylpenicillamine (SNAP) was shown to kill purified cardiac myocytes in a dose-dependent fashion. In situ analysis of ventricular myocytes plated on chamber slides using nick-end labeling of DNA demonstrated that SNAP induces cardiac myocyte apoptosis, which was confirmed by the identification of oligonucleosomal DNA fragmentation on agarose gel electrophoresis. Similarly, treatment of cardiac myocytes with cytokines that induce inducible NO synthase was shown to cause an NO-dependent induction of apoptosis. Addition of reduced hemoglobin to scavenge NO liberated by SNAP extinguished both the increase in percentage of apoptotic cells and the appearance of DNA ladders. Treatment with SNAP (but not with N-acetylpenicillamine or SNAP + hemoglobin) not only induced apoptosis but resulted in a marked increase in p53 expression in cardiac myocytes detected by Western blotting and immunohistochemistry. These data indicate that NO has the capacity to kill cardiac myocytes by triggering apoptosis and suggest the involvement of p53 in this process. p53; S-nitroso-N-acetylpenicillamine

Background and aims Pain is common in older adults but may be undertreated in part due to concerns about medication toxicity. Analgesics may affect cognition. In this retrospective cohort study, we used the Alzheimer's Disease Neuroimaging Initiative (ADNI) database to examine the interaction of cognitive status and medications, especially non-steroidal anti-inflammatory drugs (NSAIDs). We hypothesized NSAID use would be associated with cognition and that this could be mediated through changes in brain structure. Methods In this post hoc analysis of the ADNI database, subjects were selected by searching the “concurrent medications log” for analgesic medications. Subjects were included if the analgesic was listed on the medication log prior to enrollment in ADNI and throughout the study. Subjects taking analgesics, particularly NSAIDs, at each study visit were compared to control subjects taking no analgesics. Using descriptive statistics as well as univariate, multivariate and repeated measure ANOVA, we explored the relationship between NSAID use and scores for executive function and memory related cognitive activities. We further took advantage of the extensive magnetic resonance imaging (MRI) data available in ADNI to test whether cognitive change was associated with brain structure. The multitude of imaging variables was compressed into a small number of features (five eigenvectors (EV)) using principal component analysis. Results There were 87 NSAID users, 373 controls, and 71 taking other analgesics. NSAID use was associated with higher executive function scores for cognitively normal (NL) subjects as well as subjects with mild cognitive impairment (MCI). NSAID use was also associated with higher memory scores, but for NL females only. We analysed MRI data using principal component analysis to generate a set of five EVs. Examining NL and MCI subjects, one EV had significantly larger values in subjects taking NSAIDs versus control. This EV was one of two EVs which significantly correlated with composite executive function and memory scores as well as cognitive diagnosis. Conclusions NSAID use was associated with higher executive function, and memory scores in certain subjects and larger cortical volumes in particular regions. Limitations of the study include secondary analysis of existing data and the possibility of confounding. Implications These results suggest it is important to consider the secondary effects of medications when choosing a treatment regimen. Further prospective studies are needed to examine the role of analgesics on cognition and whether NSAIDs act through cortical dimension changes and how they are related to gender and cognitive diagnosis. [ABSTRACT FROM AUTHOR]

Peripherally inserted central catheters are used increasingly in the recovery of trauma and other patients. There is little data on the use and complications of these catheters in trauma patients. This retrospective review examines the rate of catheter-related thrombosis and infection in the trauma patient population at a level II trauma center over a 1-year period. Of the 27 patients who had peripherally inserted central catheters during this period, 3 (11%) developed upper extremity deep venous thrombosis and none (0%) developed catheter-associated infection. Further examination is warranted to evaluate the safety of these catheters relative to other means of intravenous access. [ABSTRACT FROM AUTHOR]