Predicting the Transfer Efficiency of Stencil Printing by Machine Learning Technique

Experiment was carried out for acquiring data regarding the transfer efficiency of stencil printing, and a machine learning-based technique (artificial neural network) was trained for predicting that parameter. The input parameters space in the experiment included the printing speed at five different levels (between 20 and120 mm/s) and the area ratio of stencil apertures from 0.34 to1.69. Three types of lead-free solder paste were also investigated as follows: Type-3 (particle size range is 20–45 μm), Type-4 (20–38 μm), Type-5 (10–25 μm). The output parameter space included the height and the area of the print deposits and the respective transfer efficiency, which is the ratio of the deposited paste volume to the aperture volume. Finally, an artificial neural network was trained with the empirical data using the Levenberg–Marquardt training algorithm. The optimal tuning factor for the fine-tuning of the network size was found to be approximately 9, resulting in a hidden neuron number of 160. The trained network was able to predict the output parameters with a mean average percentage error (MAPE) lower than 3%. Though, the prediction error depended on the values of the input parameters, which is elaborated in the paper in details. The research proved the applicability of machine learning techniques in the yield prediction of the process of stencil printing

Comparison of echocardiography and gated equilibrium radionuclide ventriculography in the measurements of left ventricular systolic function parameters in healthy dogs

Left ventricular systolic function was assessed in 12 healthy dogs with equilibrium radionuclide ventriculography. The results of the analysis were compared to traditional echocardiographic measurements. Left ventricular internal dimensions and volume were measured at the time of end-systole and end-diastole. Ejection fraction - one of the most informative parameters of cardiac function - was calculated in each animal. Values (e.g. EDD, ESD, EDV, ESV) measured by the scintigraphic method were significantly (Student's t-test, P < 0.05) higher than the data obtained by echocardiography. Ejection fraction (EF) was the only parameter that did not differ significantly when comparing the two imaging techniques. The difference between the results of parallel measurements was in inverse ratio to the size of the heart

Cluster Observations of Magnetic Field Fluctuations in the High-Altitude Cusp

High-resolution (22 vector/s) magnetic field data from Cluster FGM instrument are presented for the highaltitude cusp crossing on 17 March 2001. Despite the quiet solar wind conditions, the cusp was filled with magnetic field turbulence for much of the crossing. Large-scale fluctuations show some correlation between spacecraft but the higher frequency fluctuations show no correlation, indicating that the length scales of these waves are smaller than the spacecraft separation (500 km). In many intervals, there are clear peaks in the wave power around the ion cyclotron frequency (~1 Hz), and there is some evidence for waves at the first harmonic of this frequency. Both left- and right-hand polarised waves are found, with angles of propagation with respect to the ambient magnetic field that range from parallel to perpendicular. The regions of enhanced magnetic field fluctuations appear to be associated with plasma flows possibly originating from a lobe reconnection site. The most coherent, long lasting wave trains with frequencies close to local ion cyclotron frequency occur at a boundary between a sheared flow and a stagnant plasma

Synthesis of recyclable tire additives via equilibrium ring-opening metathesis polymerization

Linear <i>trans</i>-polypentenamers are highly desired materials among synthetic tire additives due to their comparable physical properties to natural rubber. <i>trans</i>-Polypentenamer can be prepared by equilibrium ring-opening metathesis polymerization (ROMP) using well-defined ruthenium catalyst systems. This unique feature of the equilibrium polymerization reaction opens a way for the synthesis of durable, environmentally benign elastomers where polymers including synthetic tire additives can be synthesized and readily recycled using the same transition metal catalyst system. The addition of silica fillers significantly improves the physical properties of the composite materials in comparison to the use of polymeric material. It is also known that the structural effects and the polymer–filler surface interaction are of prime importance. Herein, we report on the synthesis of silica filler compatible recyclable polypentenamer copolymers via equilibrium ROMP of cyclopentene <b>1</b> and 4-(triethoxy)­siloxy cyclopentene <b>11</b>. It has been demonstrated that polypentenamer tire additives can be synthesized via equilibrium ROMP affording polymers with high yields (>80%) at 0 °C and can be readily depolymerized at 40 °C and/or under diluted conditions using the same metathesis catalyst systems. Furthermore, the polypentenamer can also be synthesized in neat at room temperature and at very low (10⁵) monomer/catalyst ratio. This methodology is based on the synthesis of polyolefins utilizing a ruthenium-based metathesis catalyst via equilibrium ROMP of cyclopentenes and their silylated derivatives

Shedding light on the pharmacological interactions between µ-opioid analgesics and angiotensin receptor modulators:A new option for treating chronic pain

The current protocols for neuropathic pain management include µ-opioid receptor (MOR) analgesics alongside other drugs; however, there is debate on the effectiveness of opioids. Nevertheless, dose escalation is required to maintain their analgesia, which, in turn, contributes to a further increase in opioid side effects. Finding novel approaches to effectively control chronic pain, particularly neuropathic pain, is a great challenge clinically. Literature data related to pain transmission reveal that angiotensin and its receptors (the AT1R, AT2R, and MAS receptors) could affect the nociception both in the periphery and CNS. The MOR and angiotensin receptors or drugs interacting with these receptors have been independently investigated in relation to analgesia. However, the interaction between the MOR and angiotensin receptors has not been excessively studied in chronic pain, particularly neuropathy. This review aims to shed light on existing literature information in relation to the analgesic action of AT1R and AT2R or MASR ligands in neuropathic pain conditions. Finally, based on literature data, we can hypothesize that combining MOR agonists with AT1R or AT2R antagonists might improve analgesia

On the role of peripheral sensory and gut mu opioid receptors: Peripheral analgesia and tolerance

There is growing evidence on the role of peripheral \ub5-opioid receptors (MORs) in analgesia and analgesic tolerance. Opioid analgesics are the mainstay in the management of moderate to severe pain, and their efficacy in the alleviation of pain is well recognized. Unfortunately, chronic treatment with opioid analgesics induces central analgesic tolerance, thus limiting their clinical usefulness. Numerous molecular mechanisms, including receptor desensitization, G-protein decoupling, \u3b2-arrestin recruitment, and alterations in the expression of peripheral MORs and microbiota have been postulated to contribute to the development of opioid analgesic tolerance. However, these studies are largely focused on central opioid analgesia and tolerance. Accumulated literature supports that peripheral MORs mediate analgesia, but controversial results on the development of peripheral opioid receptors-mediated analgesic tolerance are reported. In this review, we offer evidence on the consequence of the activation of peripheral MORs in analgesia and analgesic tolerance, as well as approaches that enhance analgesic efficacy and decrease the development of tolerance to opioids at the peripheral sites. We have also addressed the advantages and drawbacks of the activation of peripheral MORs on the sensory neurons and gut (leading to dysbiosis) on the development of central and peripheral analgesic tolerance

Similarity and dissimilarity in antinociceptive effects of dipeptidyl-peptidase 4 inhibitors, Diprotin A and vildagliptin in rat inflammatory pain models following spinal administration.

Dipeptidyl-peptidase 4 (DPP4) enzyme is involved in the degradation of many biologically active peptides including opioids. Its role in pain transmission is poorly elucidated. Recently we reported on the spinal antihyperalgesic effects of DPP4 inhibitors, Ile-Pro-Ile (Diprotin A) and vildagliptin in carrageenan-evoked acute inflammatory pain in rats. The present study investigated the effects of intrathecal (it.) diprotin A and vildagliptin in Complete Freund's Adjuvant- (CFA) and formalin induced pain in rats. The former assay can model the subchronic inflammatory pain condition and the later one reflects both acute tonic and inflammatory pain conditions. The involvement of opioid receptor (OR) subtypes, Y1-, and GLP1 receptors were also investigated. In CFA pain model it. diprotin A or vildagliptin dose-dependently inhibits hyperalgesia in ipsilateral while has no effect in contralateral paws. The peak effect was achieved 30 min following drug administration which was used for further analysis. Both compounds showed naltrexone reversible antihyperalgesia. Co-administration of OR-subtype-selective antagonists with diprotin A and vildagliptin revealed involvement of μ and δ > μ opioid receptors, respectively. Co-administered Y1 but not GLP1 receptor antagonists reversed the antihyperalgesic action of both DPP4 inhibitors. In touch-hypersensitivity both compounds were ineffective. In formalin test only diprotin A showed μ and δ OR-mediated antinociception and only in the 2nd phase. This effect was Y1 or GLP-1 receptor antagonist insensitive. In conclusion, diprotin A and vildagliptin display antinociception of different mechanisms of action in subchronic inflammatory pain. Furthermore, the spinal pain relay points of inflammatory pain of acute or subchronic conditions were more effectively affected by diprotin A than vildagliptin which needs future elucidation

Chronic treatment with rofecoxib but not ischemic preconditioning of the myocardium ameliorates early intestinal damage following cardiac ischemia/reperfusion injury in rats

There is some recent evidence that cardiac ischemia/reperfusion (I/R) injury induces intestinal damage within days, which contributes to adverse cardiovascular outcomes after myocardial infarction. However, it is not clear whether remote gut injury has any detectable early signs, and whether different interventions aiming to reduce cardiac damage are also effective at protecting the intestine. Previously, we found that chronic treatment with rofecoxib, a selective inhibitor of cyclooxygenase-2 (COX-2), limited myocardial infarct size to a comparable extent as cardiac ischemic preconditioning (IPC) in rats subjected to 30-min coronary artery occlusion and 120-min reperfusion. In the present study, we aimed to analyse the early intestinal alterations caused by cardiac I/R injury, with or without the above-mentioned infart size-limiting interventions. We found that cardiac I/R injury induced histological changes in the small intestine within 2 h, which were accompanied by elevated tissue level of COX-2 and showed positive correlation with the activity of matrix metalloproteinase-2 (MMP-2), but not of MMP-9 in the plasma. All these changes were prevented by rofecoxib treatment. By contrast, cardiac IPC failed to reduce intestinal injury and plasma MMP-2 activity, although it prevented the transient reduction in jejunal blood flow in response to cardiac I/R. Our results demonstrate for the first time that rapid development of intestinal damage follows cardiac I/R, and that two similarly effective infarct size-limiting interventions, rofecoxib treatment and cardiac IPC, have different impacts on cardiac I/R-induced gut injury. Furthermore, intestinal damage correlates with plasma MMP-2 activity, which may be a biomarker for its early diagnosis

Glycine transporter inhibitors

Interneurons operating with glycine neurotransmitter are involved in the regulation of pain transmission in the dorsal horn of the spinal cord. In addition to interneurons, glycine release also occurs from glial cells neighboring glutamatergic synapses in the spinal cord. Neuronal and glial release of glycine is controlled by glycine transporters (GlyTs). Inhibitors of the two isoforms of GlyTs, the astrocytic type-1 (GlyT-1) and the neuronal type-2 (GlyT-2), decrease pain sensation evoked by injuries of peripheral sensory neurons or inflammation. The function of dorsal horn glycinergic interneurons has been suggested to be reduced in neuropathic pain, which can be reversed by GlyT-2 inhibitors (Org-25543, ALX1393). Several lines of evidence also support that peripheral nerve damage or inflammation may shift glutamatergic neurochemical transmission from N-methyl-D aspartate (NMDA) NR1/NR2A receptor- to NR1/NR2B receptor-mediated events (subunit switch). This pathological overactivation of NR1/NR2B receptors can be reduced by GlyT-1 inhibitors (NFPS, Org-25935), which decrease excessive glycine release from astroglial cells or by selective antagonists of NR2B subunits (ifenprodil, Ro 25-6981). Although several experiments suggest that GlyT inhibitors may represent a novel strategy in the control of neuropathic pain, proving this concept in human beings is hampered by lack of clinically applicable GlyT inhibitors. We also suggest that drugs inhibiting both GlyT-1 and GlyT-2 non-selectively and reversibly, may favorably target neuropathic pain. In this paper we overview inhibitors of the two isoforms of GlyTs as well as the effects of these drugs in experimental models of neuropathic pain. In addition, the possible mechanisms of action of the GlyT inhibitors, i.e. how they affect the neurochemical and pain transmission in the spinal cord, are also discussed. The growing evidence for the possible therapeutic intervention of neuropathic pain by GlyT inhibitors further urges development of drugable compounds, which may beneficially restore impaired pain transmission in various neuropathic conditions

Lack of Small Intestinal Dysbiosis Following Long-Term Selective Inhibition of Cyclooxygenase-2 by Rofecoxib in the Rat

Intestinal dysbiosis is linked to numerous gastrointestinal disorders, including inflammatory bowel diseases. It is a question of debate if coxibs, selective inhibitors of cyclooxygenase (COX)-2, cause dysbiosis. Therefore, in the present study, we aimed to determine the effect of long-term (four weeks) selective inhibition of COX-2 on the small intestinal microbiota in the rat. In order to avoid mucosal damage due to topical effects and inflammation-driven microbial alterations, rofecoxib, a nonacidic compound, was used. The direct inhibitory effect of rofecoxib on the growth of bacteria was ruled out in vitro. The mucosa-sparing effect of rofecoxib was confirmed by macroscopic and histological analysis, as well as by measuring the intestinal levels of cytokines and tight junction proteins. Deep sequencing of bacterial 16S rRNA revealed that chronic rofecoxib treatment had no significant influence on the composition and diversity of jejunal microbiota. In conclusion, this is the first demonstration that long-term selective inhibition of COX-2 by rofecoxib does not cause small intestinal dysbiosis in rats. Moreover, inhibition of COX-2 activity is not likely to be responsible per se for microbial alterations caused by some coxibs, but other drug-specific properties may contribute to it