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Nowadays, an image spam i s an unsolved problem because of two reasons. One is due to the diversity of spamming tricks. The other reason is due to the evolving nature of image spam. As new spam constantly emerging, filters€ effectiveness drops over time. In this paper, we present a n effective anti-spam approach to solve the two problems. First, a novel clustering filter is proposed. By exploring the density -based clustering algorithm, the proposed filter is robust to spamming tricks. Then, we present a hierarchical framework by combining the clustering filter with other machine learning based classifiers to further improve the filtering capacity. Moreover, incremental learning mechanism is integrated to ensure the proposed framework be capable of adjusting itself to overcome new imag e spamming tricks. We evaluate the proposed framework on two public spam corpora. The experiment results show that the proposed framework achieves high precision along with low false positive rate.

This essay reveals five points in which Heidegger misreads Hegel in “Hegel’s Concept of Experience”: (1) By forcedly introducing the concept of “will”, he interprets Hegel’s phenomenology of spirit into Metaphysics of Presence; (2) interprets concepts such as “statement” and “the road of skeptics” as the process of phenomenological reduction; (3) reduces Hegel’s Sein to Seiende; (4) replaces “Contradiction” with “Ambiguity” so the active Dialectics become passive; (5) exaggerates conscious experience and puts it into a real ontology, regardless of the significance of Logic and Encyclopedia of Philosophy. By an analysis of this misreading we can find the internal connection between Heidegger’s thought and that of his philosophical forerunner, Hegel.

Elevated serine elastase activity after myocardial infarction can contribute to remodeling associated with left ventricular dilatation and dysfunction. We therefore assessed the effects of overexpressing the selective serine elastase inhibitor elafin in transgenic mice in which a myocardial infarction was caused by ligation of the left anterior descending coronary artery (LAD). Elevated serine elastase activity was observed in nontransgenic littermates as early as 6 h after LAD ligation and persisted at 4 and 7 days but not in sham-operated or elafin-overexpressing transgenic mice. Myeloperoxidase activity (index of inflammatory cells) and matrix metalloproteinase 2 were also increased but only at 4 and 7 days and only in nontransgenic mice ( P < 0.05 for both comparisons), and this increase correlated with inflammatory cell infiltration. Echocardiographic study at 4 days revealed indexes of diastolic dysfunction in nontransgenic versus elafin-overexpressing mice ( P < 0.05). Morphometric and biochemical analyses at 28 days indicated impairment in cardiac performance, with greater scar thinning and infarct expansion in nontransgenic versus elafin transgenic littermates ( P < 0.05 for all comparisons). Thus serine elastase inhibition appears to suppress inflammation, cardiac dilatation, and dysfunction after myocardial infarct.

Glucagon-like peptide-1 (GLP-1) acts via its G protein-coupled receptor (GLP-1R) to regulate blood glucose. Although the GLP-1R is widely expressed in peripheral tissues, including the heart, and exogenous GLP-1 administration increases heart rate and blood pressure in rodents, the physiological importance of GLP-1R action in the cardiovascular system remains unclear. We now show that 2-month-old mice with genetic deletion of the GLP-1R (GLP-1R(-/-)) exhibit reduced resting heart rate and elevated left ventricular (LV) end diastolic pressure compared with CD-1 wild-type controls. At the age of 5 months, echocardiography and histology demonstrate increased LV thickness in GLP-1R(-/-) mice. Although baseline hemodynamic parameters of GLP-1R(-/-) did not differ significantly from those of wild type, GLP-1R(-/-) mice displayed impaired LV contractility and diastolic function after insulin administration. The defective cardiovascular response to insulin was not attributable to a generalized defect in the stress response, because GLP-1R(-/-) mice responded appropriately to insulin with increased c-fos expression in the hypothalamus and increased circulating levels of glucagon and epinephrine. Furthermore, LV contractility after exogenous epinephrine infusion was also reduced in GLP-1R(-/-) mice. These findings provide new evidence implicating an essential role for GLP-1R in the control of murine cardiac structure and function in vivo.

Inhibiting activity of the c-Myb transcription factor attenuates G 1 to S phase cell cycle transitions in vascular smooth muscle cells (SMCs) in vitro. To determine the effects of arterial SMC-specific expression of a dominant-negative c-Myb molecule ( Myb-Engrailed ) on vascular remodeling in vivo, we performed carotid artery wire-denudation in 2 independent lines of binary transgenic mice with SM22α promoter-defined Doxycycline-suppressible expression of Myb-Engrailed . Adult mice with arterial SMC-specific expression of Myb-Engrailed were overtly normal in appearance and did not display any changes in cardiovascular structure or physiology. However, bromodeoxyuridine-defined arterial SMC proliferation, neointima formation, medial hyperplasia, and arterial remodeling were markedly decreased in mice expressing arterial SMC-restricted Myb-Engrailed after arterial injury. These data suggest that c-Myb activity in arterial SMCs is not essential for arterial structure or function during development, but is involved in the proliferation of arterial SMCs as occurs in vascular pathology, and that the expression of a dominant-negative c-Myb can dramatically reduce adverse arterial remodeling in an in vivo model of restenosis. As such, this model represents a novel tissue-specific strategy for the potential gene therapy of diseases characterized by arterial SMC proliferation.

We cloned a rat vascular chymase (RVCH) from smooth muscle cells (SMCs) that converts angiotensin I to II and is up-regulated in SMC from spontaneously hypertensive vs. normotensive rats. To determine whether increased activity of RVCH is sufficient to cause hypertension, transgenic mice were generated with targeted conditional expression of RVCH to SMC, with the use of the tetracycline-controlled transactivator (tTA). We confirmed conditional expression of RVCH by mRNA, protein, and chymase activity in the absence, but not in the presence, of dietary doxycycline. The systolic blood pressure (mmHg), measured by carotid artery cannulation at 10–12 weeks of age, was higher in tTA+/RVCH+ mice than in nonbinary transgenic littermates (136 ± 4 vs. 109 ± 3) ( P < 0.05), as were the diastolic and mean pressures. Hypertension was completely reversed by doxycycline, suggesting a causal link with chymase expression. Medial thickening of mesenteric arteries from tTA+/RVCH+ mice vs. littermates (0.82 ± 0.1 vs. 0.42 ± 0.02) ( P < 0.05) was associated with increased SMC proliferation, as judged by positive immunoreactivity, with the use of an antibody to the proliferating cell nuclear antigen. These structural changes were prevented by doxycycline. Perfusion myography of mesenteric arteries from tTA+/RVCH+ mice also revealed increased vasoconstriction in response to phenylephrine and impaired metacholine-induced vasodilatation when compared with littermate controls or with the doxycyline-treated group. Our studies suggest that up-regulation of this vascular chymase is sufficient to cause a hypertensive arteriopathy, and that RVCH may be a candidate gene and a therapeutic target in patients with high blood pressure.

Serine elastases degrade elastin, stimulate vascular smooth muscle cell migration and proliferation, and are associated with myocardial damage. To evaluate the impact of elastase inhibition on cardiovascular development and disease, transgenic mice were created in which the mouse preproendothelin-1 promoter was used to target elafin overexpression to the cardiovascular system. To distinguish the transgene from endogenous elafin, constructs were made incorporating a FLAG sequence; the COOH-terminus FLAG-tagged elafin construct produced a stable, functionally active gene product and was used to create transgenic mice. Consistent with endothelin expression, abundant elafin mRNA was observed in transgenic F1 embryos (embryonic day 13.5) and in adult transgenic mice heart, trachea, aorta, kidney, lung, and skin, but not in liver, spleen, and intestine. Functional activity of the transgene was confirmed by heightened myocardial elastase inhibitory activity. No tissue abnormalities were detected by light microscopy or elastin content. However, injection of 10 plaque-forming units (PFU) of encephalomyocarditis virus resulted in death within 11 days in 10 out of 12 nontransgenic mice compared with one out of nine transgenic littermates. This reduced mortality was associated with better cardiac function and less myocardial inflammatory damage. Thus, elafin expression may confer a protective advantage in myocarditis and other inflammatory diseases.

In this letter, a novel voltage control oscillator (VCO) is proposed and fabricated by low-temperature co-fired ceramic (LTCC) technology. Advanced three-dimensional packaging structure is utilized for size reduction by embedding passive components in multilayer substrate. According to the single π circuit configuration, the models of embedded helical inductors and coupling capacitors are established to optimize the match circuit of the VCO module. With the passive components embedded into multilayer ceramic substrate, the LTCC VCO exhibits advantages of small size and high reliability compared to conventional VCO module on PCB substrate. This proposed structural model is validated through actual LTCC process. Measured parameters show good performance and agree well with the EM simulation results. The physical dimension of the VCO module is only 10 mm×10 mm×1 mm, which makes it suitable for SIP communication system.

A clinically relevant rat cardiopulmonary bypass (CPB) model would be a valuable tool for investigating pathophysiological and therapeutic strategies on bypass. Previous rat CPB models have been described in the literature; however, they have many limitations, including large circuit surface area, the inability to achieve full bypass, and donor blood requirements for prime. Therefore, we have established a rat CPB model designed to overcome these limitations. The miniature circuit consisted of a filtered reservoir, heat exchanger, membrane oxygenator (surface area = 0.02 m2) with a static priming volume of 2.8 mL, and an inline blood gas monitor. The circuit was primed with 9.5+/-0.5 mL of crystalloid solution and CPB was established on male Sprague-Dawley rats (430-475 g, n = 5) by cannulating the left common carotid artery and the right external jugular vein. The animals were placed on CPB at full flow (111+/-13 mL/kg/ min) for 1 hour and were monitored for and additional 2 hours after the CPB procedure. Hemodynamics, hemoglobin concentration (Hb), and blood gases were analyzed at three time intervals: before, during, and after CPB. The circuit performance was evaluated according to prime volume, compliance, hemodynamic parameters, and gas and heat exchange as described by modified AMMI standards. Data are expressed as mean+/-SD and a repeated-measures analysis of variance with post-Hoc test was used for data comparison between the three time intervals. The ratio of oxygenator surface area to subject body weight for this model is comparable with that of current human adult CPB practice (0.05 m2/kg vs 0.057 m2/kg) Full CPB was achieved and we observed clinically acceptable PaO2, PaCO2, and SvO2 values (209+/-86 mmHg, 25+/-2 mmHg, 78+/-8%, respectively) while on CPB. The use of asanguinous prime did produce statistically significant Hg reduction (15.7+/-0.76 vs. 9.2+/-0.59 g/dL) comparable with clinical practice. No statistically significant differences between pre- and post-CPB hemodynamics and blood gases were found in our study. We have established a miniature circuit consisting of asanquineous prime for a rat CPB model that maintains clinically acceptable results regarding hemodynamic parameters, blood gases, and hemodilution. This model would be valuable for further use in clinically relevant research studies.

In vascular smooth muscle cells (SMCs), several mechanisms act in concert to regulate the intracellular calcium concentration [Ca 2+ ] i , which may in turn affect vascular tone. One such mechanism is the extrusion of Ca 2+ by the plasma membrane calcium ATPase (PMCA). To address, in particular, the role of the neuronal nitric oxide synthase (nNOS)-associating isoform PMCA4b in regulating vascular tone, a doxycycline-responsive transgene for human PMCA4b was overexpressed in arterial SMCs of mice. Overexpression of hPMCA4b resulted in a 2-fold increase in total aortic PMCA4 protein expression and significant real-time RT-PCR-documented differences in the levels of endogenous mouse PMCA1, PMCA4, SERCA2, and IP3R1 gene expression in arterial SMCs. Whereas no significant difference in basal [Ca 2+ ] i or Ca 2+ sensitivity was observed in vascular SMCs or mesenteric arteries, respectively, from hPMCA4b-overexpressing versus control mice, hPMCA4b-overexpressing mice revealed a reduced set-point and increased extent of myogenic response and heightened sensitivity to vasoconstrictors. Treatment of arteries with an nNOS inhibitor resulted in a reduced set-point and increased extent of the myogenic response in control but not hPMCA4b-overexpressing mice. Moreover, aortic SMCs from hPMCA4b-overexpressing mice exhibited reduced levels of cGMP under both basal and phenylephrine-stimulated conditions. These changes were associated with significant doxycycline-reversible elevations in blood pressure. Taken together, these data show that overexpression of hPMCA4b in arterial SMCs increases vascular reactivity and blood pressure, an effect that may be mediated in part by negative regulation of nNOS.

The myogenic response (MR) may represent an important physiological parameter underlying arterial blood pressure (BP). We studied the effects of age, gender, and BP on the MR of mesenteric arteries from 8- to 52-wk-old mice. Increasing age and BP are associated with an increase in the perfusion pressure at which tone develops (myogenic set point). An inverse correlation exists between age and extent (magnitude) of the MR in male ( r 2 = 0.93, P = 0.0087) and female mice ( r 2 = 0.90, P = 0.013) as well as between BP and extent of the MR in male ( r 2 = 0.96, P = 0.0036) and female ( r 2 = 0.90, P = 0.014) mice. In contrast, the strength of the MR (slope of active diameter-pressure relationship) and phenylephrine-mediated constriction did not differ among these groups. Although gender had no effect on MR at any perfusion pressure or age, only male mice showed significant salt-induced hypertension and an associated increase in the set point and reduction in the extent of the MR. The set point and extent of the MR is linked to the in vivo pressure during development and experimental hypertension.

Previous studies have established that reductions in repolarizing currents occur in heart disease and can contribute to life-threatening arrhythmias in myocardium. In this study, we investigated whether the thyroid hormone analog 3,5-diiodothyropropionic acid (DITPA) could restore repolarizing transient outward K+ current ( I to) density and gene expression in rat myocardium after myocardial infarction (MI). Our findings show that I to density was reduced after MI (14.0 ± 1.0 vs. 10.2 ± 0.9 pA/pF, sham vs. post-MI at +40 mV). mRNA levels of Kv4.2 and Kv4.3genes were decreased but Kv1.4 mRNA levels were increased post-MI. Corresponding changes in Kv4.2 and Kv1.4 protein were also observed. Chronic treatment of post-MI rats with 10 mg/kg DITPA restored I to density (to 15.2 ± 1.1 pA/pF at +40 mV) as well as Kv4.2 and Kv1.4 expression to levels observed in sham-operated controls. Other membrane currents (Na+, L-type Ca2+, sustained, and inward rectifier K+ currents) were unaffected by DITPA treatment. Associated with the changes in I toexpression, action potential durations (current-clamp recordings in isolated single right ventricular myocytes and monophasic action potential recordings from the right free wall in situ) were prolonged after MI and restored with DITPA treatment. Our results demonstrate that DITPA restores I to density in the setting of MI, which may be useful in preventing complications associated with I to downregulation.