Bulk micro-defect detection with low-angle illumination.

The detection of oxygen precipitates, voids, and other defects is critical for semiconductor wafer makers. One of the industry standard techniques for detecting these Bulk Micro-Defects (BMDs) is Semilab's Light Scattering Tomograph (LST) system. In this measurement, unpatterned wafers are nominally cleaved in half. Illumination is applied to the front surface of the sample, and the light scattered off of the defects is collected via the cleaved surface. This technique had been limited to the measurement of unpatterned wafers, but device makers show significant interest in measuring BMD distributions on patterned wafers using scattering-based techniques. A pattern on the surface of the wafer can cause significant scattering, making the standard LST technique unsuitable for this task. We present a solution for patterned wafer BMD measurements by an addition of a low-angle illumination unit to the standard LST system. This new illumination unit focuses the light into the bulk of the wafer via the cleaved surface, which enables measurement on patterned samples. The new system is called "light scattering tomograph enhanced by low-angle illumination." Excellent correlation was found between the detected defect densities obtained by the low-angle and the standard LST illumination mode.

Mitochondrial protective effects of PARP-inhibition in hypertension-induced myocardial remodeling and in stressed cardiomyocytes.

AIMS: During oxidative stress mitochondria become the main source of endogenous reactive oxygen species (ROS) production. In the present study, we aimed to clarify the effects of pharmacological PARP-1 inhibition on mitochondrial function and quality control processes. MAIN METHODS: L-2286, a quinazoline-derivative PARP inhibitor, protects against cardiovascular remodeling and heart failure by favorable modulation of signaling routes. We examined the effects of PARP-1 inhibition on mitochondrial quality control processes and function in vivo and in vitro. Spontaneously hypertensive rats (SHRs) were treated with L-2286 or placebo. In the in vitro model, 150 µM H2O2 stress was applied on neonatal rat cardiomyocytes (NRCM). KEY FINDINGS: PARP-inhibition prevented the development of left ventricular hypertrophy in SHRs. The interfibrillar mitochondrial network were less fragmented, the average mitochondrial size was bigger and showed higher cristae density compared to untreated SHRs. Dynamin related protein 1 (Drp1) translocation and therefore the fission of mitochondria was inhibited by L-2286 treatment. Moreover, L-2286 treatment increased the amount of fusion proteins (Opa1, Mfn2), thus preserving structural stability. PARP-inhibition also preserved the mitochondrial genome integrity. In addition, the mitochondrial biogenesis was also enhanced due to L-2286 treatment, leading to an overall increase in the ATP production and improvement in survival of stressed cells. SIGNIFICANCE: Our results suggest that the modulation of mitochondrial dynamics and biogenesis can be a promising therapeutical target in hypertension-induced myocardial remodeling and heart failure.

Mycotoxin-degradation profile of Rhodococcus strains.

Mycotoxins are secondary fungal metabolites that may have mutagenic, carcinogenic, cytotoxic and endocrine disrupting effects. These substances frequently contaminate agricultural commodities despite efforts to prevent them, so successful detoxification tools are needed. The application of microorganisms to biodegrade mycotoxins is a novel strategy that shows potential for application in food and feed processing. In this study we investigated the mycotoxin degradation ability of thirty-two Rhodococcus strains on economically important mycotoxins: aflatoxin B1, zearalenone, fumonisin B1, T2 toxin and ochratoxin A, and monitored the safety of aflatoxin B1 and zearalenone degradation processes and degradation products using previously developed toxicity profiling methods. Moreover, experiments were performed to analyse multi-mycotoxin-degrading ability of the best toxin degrader/detoxifier strains on aflatoxin B1, zearalenone and T2 toxin mixtures. This enabled the safest and the most effective Rhodococcus strains to be selected, even for multi-mycotoxin degradation. We concluded that several Rhodococcus species are effective in the degradation of aromatic mycotoxins and their application in mycotoxin biodetoxification processes is a promising field of biotechnology.

Decreased plasma nociceptin/orphanin FQ levels after acute coronary syndromes.

Foregoing researches made on the N/OFQ system brought up a possible role for this system in cardiovascular regulation. In this study we examined how N/OFQ levels of the blood plasma changed in acute cardiovascular diseases. Three cardiac patient groups were created: enzyme positive acute coronary syndrome (EPACS, n = 10), enzyme negative ACS (ENACS, n = 7) and ischemic heart disease (IHD, n = 11). We compared the patients to healthy control subjects (n = 31). We found significantly lower N/OFQ levels in the EPACS [6.86 (6.21-7.38) pg/ml], ENACS [6.97 (6.87-7.01) pg/ml and IHD groups [7.58 (7.23-8.20) pg/ml] compared to the control group [8.86 (7.27-9.83) pg/ml]. A significant correlation was detected between N/OFQ and white blood cell count (WBC), platelet count (PLT), creatine kinase (CK), glutamate oxaloacetate transaminase (GOT) and cholesterol levels in the EPACS group.Decreased plasma N/OFQ is closely associated with the presence of acute cardiovascular disease, and the severity of symptoms has a significant negative correlation with the N/OFQ levels. We believe that the rate of N/OFQ depression is in association with the level of ischemic stress and the following inflammatory response. Further investigations are needed to clarify the relevance and elucidate the exact effects of the ischemic stress on the N/OFQ system.

Physical and physiological performances in 10-year-old obese boys.

Fatness generally has a negative influence on the performance of a variety of motor and cardiorespiratory fitness tests. The aim of this comparison was to analyse the effects of three grades of obesity on somatic growth, physical performance and oxygen consumption during exercise. Volunteer boys with definitely different grades of obesity were recruited for the comparison. In the group of mildly obese children (G1; n=23) BMI ranged between 24 kg.m -2 and 26 kg.m -2 ; and individual percent body fat was between 33% and 33.5%. In the case of moderate obesity (G2; n=23) BMI ranged between 26.5 kg.m -2 and 28.5 kg.m -2 ; and percent body fat was between 35% and 36%. In the extremely obese group (G3; n=20) BMI was greater than 31 kg.m -2 ; percent body fat was greater than 37.5%. Oxygen consumption during the 1,200 m run-test was measured by VIMEX-ST-type (USA) telemetric equipment.The greatest absolute aerobic power referred to the G3 boys, and the lowest oxygen consumption was characteristic of the mildly obese group. The very high differences between the body mass means resulted in a more marked inter-group variability in mean relative oxygen uptake.The predicted relative fat and high body fat content observed on the trunk, and the elevated level of resting blood pressure may indicate serious risks for the development of cardio-respiratory and metabolic disease. The very low oxygen consumption relative to body mass and poor physical performance are expected consequences of physiologic and environmental influences on the obese population.

Epidural anesthesia? No of course.

Although the contraindications for thoracic epidural anesthesia (TEA) are well defined, the debate continues about whether TEA improves outcomes. Pro and con trials and a metaanalysis in the past have yielded equivocal results; they did not deal with new vascular intervention or drugs. The benefit of TEA in surgery is to provide analgesia. In subgroups, TEA can decrease the mortality and morbidity. In contrast, the cost can increase in the situation of a complication that is opposite to the side effects is rare, but the impairment caused by them is out of proportion to the benefits. Primary or secondary prophylaxis with antithrombotic drugs is increasing in developed countries because of the increasing cardiovascular interventions and aging of the population. The neuroaxial guidelines are useful, but the changing of the coagulation profile after hepatectomy is not included in them. The decision to use TEA in liver surgery must be individualized with steps planned from the beginning. TEA suitability is based on an evaluation of the contraindications, comorbidities, coagulation profiles, hepatic reserve, and balance of benefits and risks. The insertion or withdrawal of the epidural catheter should be made with care according to the neuroaxial guidelines and in the presence of a normal TEG. The decreasing level of prothrombin content and platelet counts after hepatectomy should be closely monitored every 2 to 5 days.

Evaluation of liver function for hepatic resection.

New limits have been established to decrease mortality and morbidity rates after liver resection in cirrhotic and non-cirrhotic patients. Various laboratory data and imaging techniques have been used to complement the Child-Pugh score to predict liver failure after hepatectomy and to assess functional hepatic reserve. The greatest experiences are with the aminopyrine breath test and the galactosyl elimination capacity, which are decreased among hepatic failure patients after liver resection. However, absence of these changes do not totally exclude it. The indocyanine green retention test is the most widely used clearance test. Nevertheless, it remains imperfect because it depends both on hepatic blood flow and on the functional capacity of the liver. Nuclear imaging of the asialoglicoprotein receptors with radiolabelled synthetic asialoglicoproteins provides volumetric information as well a functional assessment of the liver. In summary, while liver function is complex, a successful liver test to assess quantitative functional hepatic reserve still needs to be established. The combination of the Child-Pugh score, the presence of ascites, the serum bilirubin levels, the indocyanine green retention (ICG R15) value, and the remnant liver CT volumetry seems to avoid an index of liver failure after hepatic resection. Cases when ICG R15 is above 15% should be combined with portal vein embolization. If there is no possibility to perform an ICG clearance test, it may be replaced with other available, well known dynamic liver function tests.

Synaptic reorganization of calbindin-positive neurons in the human hippocampal CA1 region in temporal lobe epilepsy.

The distribution, morphology, synaptic coverage and postsynaptic targets of calbindin-containing interneurons and afferent pathways have been analyzed in the control and epileptic CA1 region of the human hippocampus. Numerous calbindin-positive interneurons are preserved even in the strongly sclerotic CA1 region. The morphology of individual cells is altered: the cell body and dendrites become spiny, the radially oriented dendrites disappear, and are replaced by a large number of curved, distorted dendrites. Even in the non-sclerotic epileptic samples, where pyramidal cells are present and calbindin-immunoreactive interneurons seem to be unchanged, some modifications could be observed at the electron microscopic level: they received more inhibitory synaptic input, and the calbindin-positive excitatory afferents - presumably derived from the CA1, the CA2 and/or the dentate gyrus - are sprouted. In the strongly sclerotic tissue, with the death of pyramidal cells, calbindin-positive terminals (belonging to interneurons and the remaining excitatory afferents) change their targets. Our data suggest that an intense synaptic reorganization takes place in the epileptic CA1 region, even in the non-sclerotic tissue, before the death of considerable numbers of pyramidal cells. Calbindin-positive interneurons participate in this reorganization: they show plastic changes in response to epilepsy. The enhanced inhibition of inhibitory interneurons may result in the disinhibition of pyramidal cells or in an abnormal synchrony in the output region of the hippocampus.