679 research outputs found
Increasing the biosafety of analytical systems in the clinical laboratory
Biosafety is an important part of the know-how of all clinical
laboratory professionals. Biosafely must have high priority in the
design and use of analytical systems. Attention should be focused
on reducing the handling of biological specimens, reducing
biohazards to laboratory personnel, and on improving the labelling
and containment of biohazardous materials. In this paper, biosafety
issues are discussed in relation to the design of analytical systems,
their use and maintenance
Is attending a mental process?
The nature of attention has been the topic of a lively research programme in psychology for over a century. But there is widespread agreement that none of the theories on offer manage to fully capture the nature of attention. Recently, philosophers have become interested in the debate again after a prolonged period of neglect. This paper contributes to the project of explaining the nature of attention. It starts off by critically examining Christopher Mole’s prominent “adverbial” account of attention, which traces the failure of extant psychological theories to their assumption that attending is a kind of process. It then defends an alternative, process-based view of the metaphysics of attention, on which attention is understood as an activity and not, as psychologists seem to implicitly assume, an accomplishment. The entrenched distinction between accomplishments and activities is shown to shed new light on the metaphysics of attention. It also provides a novel diagnosis of the empirical state of play
Round-robin analysis of the RILEM TC 162-TDF-beam-bending test. Part 2 - Approximation of d from the CMOD response
Sensitivity of northeastern US surface ozone predictions to the representation of atmospheric chemistry in the Community Regional Atmospheric Chemistry Multiphase Mechanism (CRACMMv1.0)
Chemical mechanisms describe how emissions of gases and particles evolve in
the atmosphere and are used within chemical transport models to evaluate
past, current, and future air quality. Thus, a chemical mechanism must
provide robust and accurate predictions of air pollutants if it is to be
considered for use by regulatory bodies. In this work, we provide an initial
evaluation of the Community Regional Atmospheric Chemistry Multiphase
Mechanism (CRACMMv1.0) by assessing CRACMMv1.0 predictions of surface ozone
(O3) across the northeastern US during the summer of 2018 within the
Community Multiscale Air Quality (CMAQ) modeling system. CRACMMv1.0 O3
predictions of hourly and maximum daily 8 h average (MDA8) ozone were
lower than those estimated by the Regional Atmospheric Chemistry Mechanism with aerosol module 6
(RACM2_ae6), which better matched surface network
observations in the northeastern US (RACM2_ae6 mean bias of
+4.2 ppb for all hours and +4.3 ppb for MDA8; CRACMMv1.0 mean bias of
+2.1 ppb for all hours and +2.7 ppb for MDA8). Box model calculations
combined with results from CMAQ emission reduction simulations indicated
a high sensitivity of O3 to compounds with biogenic sources. In addition,
these calculations indicated the differences between CRACMMv1.0 and
RACM2_ae6 O3 predictions were largely explained by
updates to the inorganic rate constants (reflecting the latest assessment
values) and by updates to the representation of monoterpene chemistry.
Updates to other reactive organic carbon systems between
RACM2_ae6 and CRACMMv1.0 also affected ozone predictions and
their sensitivity to emissions. Specifically, CRACMMv1.0 benzene, toluene,
and xylene chemistry led to efficient NOx cycling such that CRACMMv1.0 predicted controlling aromatics reduces ozone without rural O3
disbenefits. In contrast, semivolatile and intermediate-volatility alkanes
introduced in CRACMMv1.0 acted to suppress O3 formation across the
regional background through the sequestration of nitrogen oxides (NOx)
in organic nitrates. Overall, these analyses showed that the CRACMMv1.0 mechanism within the CMAQ model was able to reasonably simulate ozone
concentrations in the northeastern US during the summer of 2018 with similar
magnitude and diurnal variation as the current operational Carbon Bond
(CB6r3_ae7) mechanism and good model performance compared to recent
modeling studies in the literature.</p
Regulation of Epithelial Cell Morphology and Functions Approaching To More In Vivo-Like by Modifying Polyethylene Glycol on Polysulfone Membranes
Cytocompatibility is critically important in design of biomaterials for application in tissue engineering. However, the currently well-accepted “cytocompatible" biomaterials are those which promote cells to sustain good attachment/spreading. The cells on such materials usually lack the self-assembled cell morphology and high cell functions as in vivo. In our view, biomaterials that can promote the ability of cells to self-assemble and demonstrate cell-specific functions would be cytocompatible. This paper examined the interaction of polyethylene glycol (PEG) modified polysulfone (PSf) membranes with four epithelial cell types (primary liver cells, a liver tumor cell line, and two renal tubular cell lines). Our results show that PSf membranes modified with proper PEG promoted the aggregation of both liver and renal cells, but the liver cells more easily formed aggregates than the renal tubular cells. The culture on PEG-modified PSf membranes also enhanced cell-specific functions. In particular, the cells cultured on F127 membranes with the proper PEG content mimicked the in vivo ultrastructure of liver cells or renal tubules cells and displayed the highest cell functions. Gene expression data for adhesion proteins suggest that the PEG modification impaired cell-membrane interactions and increased cell-cell interactions, thus facilitating cell self-assembly. In conclusion, PEG-modified membrane could be a cytocompatible material which regulates the morphology and functions of epithelial cells in mimicking cell performance in vivo
The assessment of neuromuscular fatigue during 120 min of simulated soccer exercise
Purpose
This investigation examined the development of neuromuscular fatigue during a simulated soccer match incorporating a period of extra time (ET) and the reliability of these responses on repeated test occasions.
Methods
Ten male amateur football players completed a 120 min soccer match simulation (SMS). Before, at half time (HT), full time (FT), and following a period of ET, twitch responses to supramaximal femoral nerve and transcranial magnetic stimulation (TMS) were obtained from the knee-extensors to measure neuromuscular fatigue. Within 7 days of the first SMS, a second 120 min SMS was performed by eight of the original ten participants to assess the reliability of the fatigue response.
Results
At HT, FT, and ET, reductions in maximal voluntary force (MVC; −11, −20 and −27%, respectively, P ≤ 0.01), potentiated twitch force (−15, −23 and −23%, respectively, P < 0.05), voluntary activation (FT, −15 and ET, −18%, P ≤ 0.01), and voluntary activation measured with TMS (−11, −15 and −17%, respectively, P ≤ 0.01) were evident. The fatigue response was robust across both trials; the change in MVC at each time point demonstrated a good level of reliability (CV range 6–11%; ICC2,1 0.83–0.94), whilst the responses identified with motor nerve stimulation showed a moderate level of reliability (CV range 5–18%; ICC2,1 0.63–0.89) and the data obtained with motor cortex stimulation showed an excellent level of reliability (CV range 3–6%; ICC2,1 0.90–0.98).
Conclusion
Simulated soccer exercise induces a significant level of fatigue, which is consistent on repeat tests, and involves both central and peripheral mechanisms
Different levels of hsp70 and hsc70 mRNA expression in Iberian fish exposed to distinct river conditions
PTTG1 Attenuates Drug-Induced Cellular Senescence
As PTTG1 (pituitary tumor transforming gene) abundance correlates with adverse outcomes in cancer treatment, we determined mechanisms underlying this observation by assessing the role of PTTG1 in regulating cell response to anti-neoplastic drugs. HCT116 cells devoid of PTTG1 (PTTG1−/−) exhibited enhanced drug sensitivity as assessed by measuring BrdU incorporation in vitro. Apoptosis, mitosis catastrophe or DNA damage were not detected, but features of senescence were observed using low doses of doxorubicin and TSA. The number of drug-induced PTTG1−/− senescent cells increased ∼4 fold as compared to WT PTTG1-replete cells (p<0.001). p21, an important regulator of cell senescence, was induced ∼3 fold in HCT116 PTTG1−/− cells upon doxorubicin or Trichostatin A treatment. Binding of Sp1, p53 and p300 to the p21 promoter was enhanced in PTTG1−/− cells after treatment, suggesting transcriptional regulation of p21. p21 knock down abrogated the observed senescent effects of these drugs, indicating that PTTG1 likely suppresses p21 to regulate drug-induced senescence. PTTG1 also regulated SW620 colon cancer cells response to doxorubicin and TSA mediated by p21. Subcutaneously xenografted PTTG1−/− HCT116 cells developed smaller tumors and exhibited enhanced responses to doxorubicin. PTTG1−/− tumor tissue derived from excised tumors exhibited increased doxorubicin-induced senescence. As senescence is a determinant of cell responses to anti-neoplastic treatments, these findings suggest PTTG1 as a tumor cell marker to predict anti-neoplastic treatment outcomes
- …