Cascaded systems analysis of anatomic noise in digital mammography and dual-energy digital mammography.

In x-ray based imaging of the breast, contrast between fibroglandular (Fg) tissue and adipose (Ad) tissue is a source of anatomic noise. The goal of this work was to validate by simulation and experiment a mathematical framework for modelling the Fg component of anatomic noise in digital mammograpy (DM) and dual-energy (DE) DM. Our mathematical framework unifies and generalizes existing approaches. We compared mathematical predictions directly with empirical measurements of the anatomic noise power spectrum of the CIRS BR3D structured breast phantom using two clinical mammography systems and four beam qualities. Our simulation and experimental results showed agreement with mathematical predictions. As a demonstration of utility, we used our mathematical framework in a theoretical spectral optimization of DM for the task of detecting breast masses. Our theoretical optimization showed that the optimal tube voltage for DM may be higher than that based on predictions that do not account for anatomic noise, in agreement with recent theoretical findings. Additionally, our theoretical optimization predicts that filtering tungsten-anode x-ray spectra with rhodium has little influence on lesion detectability, in contrast with previous findings. The mathematical methods validated in this work can be incorporated easily into cascaded systems analysis of breast imaging systems and will be useful when optimizating novel techniques for x-ray-based imaging of the breast.

Effective Synthesis of Highly Oxidized Graphene Oxide That Enables Wafer-scale Nanopatterning: Preformed Acidic Oxidizing Medium Approach.

Demand for rapid and massive-scale exfoliation of bulky graphite remains high in graphene commercialization and property manipulation. We report a procedure utilizing "preformed acidic oxidizing medium (PAOM)" as a modified version of the Hummers' method for fast and reliable synthesis of graphene oxide. Pre-mixing of KMnO4 and concentrated H2SO4 prior to the addition of graphite flakes enables the formation of effectively and efficiently oxidized graphene oxide (EEGO) featured by its high yields and suspension homogeneity. PAOM expedites diffusion of the Mn-oxidants into the graphite galleries, resulting in the rapid graphite oxidation, capable of oxidizing bulky graphite flakes (~0.8 mm in diameter) that can not be realized by the Hummers' method. In the scale-up tests, ten-time amount of graphite can be completely exfoliated by PAOM without need of extended reaction time. The remarkable suspension homogeneity of EEGO can be exploited to deposit ultra-flat coating for wafer-scale nanopatterning. We successfully fabricated GO optical gratings with well-defined periodicity (300 nm) and uniform thickness (variation <7 nm). The combination of the facile and potent PAOM approach with the wafer-scale patterning technique may realize the goal for massive throughput graphene nanoelectronics.

CT radiation profile width measurement using CR imaging plate raw data.

This technical note demonstrates computed tomography (CT) radiation profile measurement using computed radiography (CR) imaging plate raw data showing it is possible to perform the CT collimation width measurement using a single scan without saturating the imaging plate. Previously described methods require careful adjustments to the CR reader settings in order to avoid signal clipping in the CR processed image. CT radiation profile measurements were taken as part of routine quality control on 14 CT scanners from four vendors. CR cassettes were placed on the CT scanner bed, raised to isocenter, and leveled. Axial scans were taken at all available collimations, advancing the cassette for each scan. The CR plates were processed and raw CR data were analyzed using MATLAB scripts to measure collimation widths. The raw data approach was compared with previously established methodology. The quality control analysis scripts are released as open source using creative commons licensing. A log-linear relationship was found between raw pixel value and air kerma, and raw data collimation width measurements were in agreement with CR-processed, bit-reduced data, using previously described methodology. The raw data approach, with intrinsically wider dynamic range, allows improved measurement flexibility and precision. As a result, we demonstrate a methodology for CT collimation width measurements using a single CT scan and without the need for CR scanning parameter adjustments which is more convenient for routine quality control work.

K(ATP) channels and MPTP are involved in the cardioprotection bestowed by chronic intermittent hypobaric hypoxia in the developing rat.

The aim of this study was to explore the mechanism underlying the cardioprotection bestowed by chronic intermittent hypobaric hypoxia (CIHH) against ischemia/reperfusion (I/R) injury in developing rats. Neonatal male rats were subjected to CIHH treatments that simulated an altitude of 3000 m a.s.l. for 28 days (CIHH28) and 42 days (CIHH42), respectively, or no treatment (control). The left ventricular function of isolated hearts was evaluated. The ultra-microstructure, superoxide dismutase (SOD) activity and total anti-oxidation capacity (TAC) of the myocardium were determined. The basic left ventricular function remained unchanged in CIHH rats, except for an increased coronary flow. The recovery of cardiac function from I/R, however, was much better in CIHH rats than in control rats. Compared to control rats, CIHH rats had much higher SOD levels and TAC, and the ultra-microstructure damage to mitochondria was considerably less. The cardiac protection of CIHH was canceled out by glibenclamide, an inhibitor of the ATP-sensitive potassium (K(ATP)) channel, 5-hydroxydecanoate, an inhibitor of mitochondrial K(ATP) (mitoKATP), and atractyloside, an opener of the mitochondrial permeability transition pore (MPTP). To the contrary, diazoxide, an opener of mitoKATP, and cyclosporin A, a blocker of MPTP opening, induced cardioprotection in control rats. These results suggest that CIHH protects the heart against I/R injury in developing rats through opening of the K(ATP) channel and inhibiting of opening of the MPTP.

Effect of chronic intermittent hypobaric hypoxia on α(1)-adrenergic receptor of myocardium participates in the cardioprotection.

The purpose of the present study was to investigate the effect of chronic intermittent hypobaric hypoxia (CIHH) on α(1)-adrenergic receptors and the role of alpha(1)-adrenergic receptors in the protection of CIHH against ischemic injury of myocardium. Sixty-six adult male Sprague-Dawley rats were randomly divided into four groups: control group (Con), 14-day CIHH treatment group (CIHH14), 28-day CIHH treatment group (CIHH28) and 42-day CIHH treatment group (CIHH42). CIHH rats were exposed to hypoxia mimicking 5 000 m altitude (p(B)=404 mmHg, p(O(2))=84 mmHg) in a hypobaric chamber, 6 h daily for 14, 28 and 42 d, respectively. Control animals lived in the same environment as CIHH animals except hypoxia exposure. After anesthesia with sodium pentobarbital (3.0-3.5 mL/kg body weight, i.p.), papillary muscle was taken from the right ventricle of rat and perfused with modified Tyrode's solution continuously, at constant temperature (37 °C) and perfusion speed (12 mL/min). Muscle contraction was evoked by electric stimuli. Different concentrations (1x10(-7), 1x10(-6) and 1x10(-5) mol/L) of phenylephrine (PE), an alpha(1)-adrenergic receptor agonist, were applied cumulatively to investigate the effect of PE on the mechanic contraction of right ventricular papillary muscles of rats in Con, CIHH14, CIHH28 and CIHH42 groups. Also, prazosin (1x10(-6) mol/L), an α(1)-adrenergic receptor antagonist, was used to investigate the role of α(1)-adrenergic receptor in the protective effect of CIHH on papillary muscle. The results showed: (1) PE increased the maximal isometric tension (P(max)) and maximal velocity of tension development (P(dT/dt)) of muscle contraction in a dose-dependent manner (P<0.05), and the increase of the muscle contraction was much greater in CIHH28 and CIHH42 rats than that in Con rats (P<0.05). Under 1x10(-5) mol/L of PE, the increases of P(max) and P(dT/dt) over the baseline were 51.2% and 44.5% in CIHH28 group, 48.6% and 44.5% in CIHH42 group, and 28.7% and 24.5% in Con group, respectively; (2) The contraction of papillary muscle decreased during simulated ischemia, but the decrease was slighter in CIHH rats than that in Con rats (P<0.05). The decreases in P(max) and P(dT/dt) were 59.6% and 53.6% in CIHH28 group, 60.4% and 49.9% in CIHH42 group, and 74.4% and 64.7% in Con group, respectively; (3) The protective effect of CIHH on ischemic papillary muscle was abolished by prazosin (1x10(-6) mol/L). The results of the present study suggest that CIHH increases the activity of α(1)-adrenergic receptor, which is possibly one of the mechanisms for the cardioprotection of CIHH.

[Effects of chronic intermittent hypobaric hypoxia on immune function in rat].

AIM: To elucidate the effect of CIHH on cellular immunity and humoral immunity in rat by using flow cytometry method, immunohistochemistry method and electron microscopy techniques. METHODS: Forty-eight male adult Sprague-Dawley rats were randomly divided into 4 groups: control(CON) group, 14 days CIHH (CIHH14) group, 28 days CIHH (CIHH28) group, 42 days CIHH (CIHH42) group. The animals in CIHH groups were exposed to 14, 28 and 42 days hypobaric hypoxia(simulated 3 000 m altitude, 5 h per day), respectively. Half of the animals in each group was treated with normaxia and the other half animals were treated with acute hypoxia for 1 h. CD3, CD4, CD8 T lymphocytes, natural killer (NK) cells, IgG, cortisol, epirenamine and C-reactive protein were examined. The weight and ultrastructure of thymus and spleen were observed. RESULTS: (1) Compared with CON, both indexes of thymus and spleen in CIHH14 rats were increased significantly. Spleen index, but not thymus index, was increased in CIHH28 and CIHH42 rats. The thymocytes and spleen cytes in rat were injuryed during acute hypoxia, but the damage in CIHH rats was significant slighter than that in CON rats. (2) Compared with CON, CIHH28 and CIHH42, CD8 in CIHH14 rats were decreased, ratios of CD4/CD8 was increased and NK was decreased. (3) The rats of CON during acute hypoxia showed that CD4 was increased, CD8 was decreased, ratio of CD4/CD8 was elevated, and NK was increased. But there were no significant changes of CD3, CD4, CD8 and NK in CIHH28 and CIHH42 animals during acute hypoxia. (4) Compared with CON, CIHH28 and CIHH42, cortisol in CIHH14 rats was increased obviously, Epirenamine, cortisol and C-reactive protein in CON rats were increased, but there were no obvious changes in CIHH rats before and after acute hypoxia. CONCLUSION: CIHH protects the immune function of rat against acute hypoxia, which is related with the regulation of neuroendocrine.

Electrochemical properties of niosomes modified Au electrode and DNA recognition.

Non-ionic surfactant vesicles (NSVs), also referred to as niosomes, have been studied as an alternative to conventional liposomes. In this paper, electrochemical inspection of the interaction between Herring sperm DNA and niosomes has been investigated after a simple and novel method for the formation of niosomes on Au electrode. Each step of electrode modification has been confirmed with cyclic voltammetry (CV) and electrochemical impedance spectroscopy (EIS). The assembly of octadecanethiol (ODT) layer on the electrode surface generates a packed film that introduces a barrier to the interfacial electron transfer (R(et)), and the subsequent immobilization of niosomes onto the self-assembled monolayer (SAM) layer results in a further increase of R(et), due to the formed bilayer almost blocked the redox probe to the electrode surface. When Herring sperm DNA was added, the R(et) value decreased, indicating that the barrier of the redox probe to the surface was disrupted. The addition of DNA caused the formation of some transmembrane channels for the redox probe across the niosomes. A good linear relationship between R(et) value and DNA concentration was found over the 0-0.05 mg mL(-1) concentration range.

Protective effect of polydatin against ischemia/reperfusion injury in rat heart.

The aim of the present study was to investigate the protective effect of polydatin against myocardial ischemia/reperfusion injury in rats and the underlying mechanism. In anesthetized rats, ischemia and reperfusion arrhythmia produced by ligating and loosing the coronary artery was recorded and myocardial infarct size was measured. In Langendorff isolated rat heart, cardiac function was recorded before and after 30 min of global ischemia followed by 60 min of reperfusion. The parameters of cardiac function include left ventricular developed pressure (LVDP), maximal differentials of LVDP (±LVdp/dt(max)) and coronary flow (CF) were measured. Myocardial superoxide dismutase (SOD) activity, the contents of myocardial malondialdehyde (MDA) and nitric oxide (NO) as well as the activity of nitric oxide synthase (NOS) were measured in isolated heart. The results showed: (1) Arrhythmia score and myocardial infarct size were significantly lower in polydatin group than that in the control group (P<0.05, P<0.01); (2) The recovery of LVDP, ±LVdp/dt(max) and CF during reperfusion in polydatin group were significantly better than that in the control rats (P<0.05, P<0.01); (3) SOD activity in polydatin group was significantly higher than that in the control group, but MDA content was lower in polydatin group than that in the control group (P<0.05); (4) NO content and NOS activity, especially constitutive nitric oxide synthase (cNOS) activity in polydatin group were higher than that in the control group (P<0.05); (5) L-NAME, the NOS inhibitor, reversed the protective effect of polydatin against ischemia/reperfusion injury. The results suggest that polydatin has a protective effect against ischemia/reperfusion injury in rat heart. The cardioprotection of polydatin is mainly mediated by cNOS which leading to an increase in NO production.

Effects of different modes of intermittent hypobaric hypoxia on ischemia/reperfusion injury in developing rat hearts.

The aim of the present study was to explore the effects of two different modes of intermittent hypobaric hypoxia (IHH) on myocardial ischemia/reperfusion injury in developing rat hearts. Postnatal male sprague-Dawley rats (n=72) were divided randomly into 3 groups: intermittent hypoxia at 3 000 m (IHH3000) group, intermittent hypoxia at 5 000 m (IHH5000) group and control group. The isolated hearts were perfused in the Langendorff apparatus, undergoing 30 min of global ischemia and 60 min of reperfusion. Cardiac function, coronary flow and lactate dehydrogenase (LDH) activity were recorded at 5 min before ischemia and 1, 5, 10, 20, 30, 60 min during reperfusion, respectively. The heart weight was measured at the end of the experiment. The results showed that: (1) There was no difference in body weight gaining between IHH3000 and control groups. The gain of body weight in IHH5000 group was much lower than that in IHH3000 and control groups (P<0.01). (2) Compared with that in the control group, the recovery of cardiac function in IHH3000 group was enhanced at 60 min after ischemia/reperfusion, coronary flow was increased, and LDH activity was decreased (P<0.05), meaning a cardioprotective effect occurred. There was no significant difference in heart weight between IHH3000 and control groups. In addition, cardiac function restored better in IHH3000 group after 42 d of hypoxic exposure than that after 28 d of hypoxic exposure (P<0.05). (3) Compared with that in the control group, the recovery of cardiac function in IHH5000 group was lower, coronary flow was decreased, and LDH activity was increased (P<0.05). There was a hypertrophy in the right ventricle in IHH5000 group. All changes indicated definitely that a detrimental effect developed in IHH5000 group. The results suggest that proper IHH can protect developing rat hearts against ischemia/reperfusion injury while this effect could be affected by the modes of intermittent hypoxic exposure.