Transient Attenuation Research Articles

Exercise‐Attenuation of Q‐Waves in II, III, and aVF, and R‐Waves in V1 and V2 in a Patient with an Inferior Infarction and Anterior Wall Ischemia

A 63-year-old male patient with inferior infarction revealed transient attenuation of the Q-waves in II, III, and aVF, and R-waves in V1-V3 during an exercise stress test. Myocardial scintigraphy disclosed ischemia of the anterior wall and coronary arteriography, a 90% stenosis of the left main coronary artery (LMCA). The mechanism involved appears to be a transient failure of the anterior wall to generate adequate depolarization forces for the genesis of Q-waves in the inferior leads and R-waves in the anterior leads. This electrocardiogram sign is diagnostic of severe anterior wall ischemia due to left anterior descending or LMCA stenosis.

Transient hepatic attenuation difference (THAD) in biliary duct disease

THADs are associated with a wide spectrum of hepato-biliary pathologies. The aim of this paper is to find out the role of THADs in the imaging assessment of biliary diseases. We performed a retrospective study to establish the frequency of arterial phenomena in patients with specific biliary diseases. Out of 1833 patients who underwent upper abdomen biphasic CT (2003-2007), we selected those with the following diagnoses: biliary duct dilation due to extrahepatic obstruction (20 patients-group A), intrahepatic-hilar cholangiocellular-carcinoma (19 patients-group B), and cholangitis (14 patients-group C). THAD presence/pattern was assessed for each group. Patients without any demonstrable clinical/imaging signs of liver/biliary pathology (1124) were the control group. THADs were observed in 36/53 (67.9%) and 20/1124 (1.78%) in study and control groups respectively, with significant association between each diagnostic group and THAD patterns (P < 0.0001). Eleven out of 20 (55%) group A patients showed peribiliary-THAD around dilated biliary tracts; 15/19 (79%) group B patients demonstrated portal involvement and sectorial-THAD; 10/14 (71%) group C patients revealed polymorphous-THAD all along inflamed biliary duct. However, THADs are complex phenomena, their evaluation can be an additional diagnostic tool in patients with a biliary pathology. Diffuse peribiliary, sectorial, and polymorphous-THADs show a good rate of correlation (P < 0.0001) with biliary duct ectasia, portal infiltration, and cholangitis, respectively.

Transient hepatic attenuation difference on computed tomography associated with hepatic epithelioid hemangioendothelioma

Hepatic epithelioid hemangioendothelioma (EHE) is a rare low-grade malignant vascular tumor with a clinical course between cavernous hemangioma and angiosarcoma. Several imaging findings have been described in EHEs. We report a case of an EHE which demonstrated an associated transient hepatic attenuation difference (THAD) on arterial-phase computed tomography examination. THAD associated with an EHE has not previously been reported. The presence of a THAD may be related to the propensity of this tumor for vascular invasion.

Transient hepatic attenuation difference (THAD) following transcatheter arterial chemoembolization for hepatic malignancy: changes on serial CT examinations

The purpose of this study was to investigate the natural history of transcatheter arterial chemoembolization (TACE)-induced, transient hepatic attenuation difference (THAD). Among the patients who underwent TACE for treatment of hepatocellular carcinomas during a 32-month period, 32 patients with 40 newly developed THADs defined as localized, transient, peripheral hepatic parenchymal enhancement during the hepatic arterial phase of dynamic CT (axial dimension, 1.9-8.8 cm; mean, 4.9 cm) in the vicinity of iodized-oil accumulation were subjected to a retrospective analysis of serial follow-up CT examinations. Among the 40 TACE-induced THADs, 18 (45%) and 9 (23%) were accompanied with arterial-portal venous fistula (APF) and portal venous stenosis (PVS), respectively, while 2 (5%) THADs showed both APF and PVS simultaneously. Thirty-eight (95%) THADs disappeared spontaneously during the follow-up period (range, 4-26 months; mean, 9 months), and 11 (29%) of them showed progressive atrophy of the corresponding hepatic parenchyma. Regardless of the presence of APF, 10 (91%) of 11 THADs of following parenchymal atrophy had shown PVSs (P<0.001). During the long-term follow-up period after TACE, almost all of the TACE-induced THADs spontaneously disappeared and either had or did not have corresponding parenchymal atrophy, which is strongly related to the presence of PVS. Understanding the nature of these CT features would be helpful for radiologists in determining the prognosis of the TACE-induced hepatic injuries as well as in distinguishing them from the recurrent tumour.

Nitric oxide synthase inhibition into the rat locus coeruleus delays the LPS‐induced fever

This work was aimed at analyzing whether nitric oxide (NO) synthesis in the rat locus coeruleus (LC) is essential for mounting the LPS‐induced fever. Male Wistar rats (320–350g) were chronically, stereotaxically implanted with one guide cannula just above the LC and had a miniature temperature datalogger (SubCue) inserted in the peritoneal cavity. Unanesthetized, freely moving rats were unilaterally microinjected into the LC with either a nonselective nitric oxide synthase (NOS) inhibitor [L‐NMMA; 50 nmol in 100 nL of pyrogen‐free saline (PFS)] or just PFS as control, and were, 30 min later, intraperitoneally injected with either a polyphasic fever‐inducing dose of bacterial lipopolysaccharide [LPS; 100 μg/kg in PFS (1 mL/kg)] or PFS (vehicle), at an isothermal, subneutral ambient temperature (23°C). Under NOS inhibition, we observed an increased latency (1 h) for the onset of fever and also a mild, transient attenuation of its second phase (F2,18=5.334; p&lt;0.001, vs control groups); a thermal index analysis showed a slighter fever (F2,18=5.482; p=0.0138, vs control groups). Moreover, measurements of LC nitrite/nitrate concentration revealed that the LC nitric oxide synthesis increased during the course of fever (p&lt;0.001, vs saline group). These results indicate that the endogenous synthesis of NO into the rat LC mediates the onset of the LPS‐induced fever. Financial support: FAPESP, CNPq.

Waiting to exhale: salvaging the nondiagnostic CT pulmonary angiogram by using expiratory imaging to improve contrast dynamics

We attempted to investigate whether computed tomography pulmonary angiography (CTPA) in the expiratory phase can improve contrast enhancement of the pulmonary arteries and mitigate the effect of inspiratory transient attenuation artifact, potentially salvaging nondiagnostic studies. Eighteen patients with indeterminate inspiratory CTPA, despite proper contrast bolus were studied. Patients were rescanned in expiration using the same contrast bolus and scanning parameters. The attenuation of each pulmonary arterial segment, superior and inferior vena cava, and atria and ventricles during the two phases of respiration was measured independently by three radiologists. All pulmonary segments were evaluated for filling defects during the two phases. In addition, the studies were graded for diagnostic quality of enhancement and probable impact on management. A statistically significant increase in pulmonary arterial enhancement was seen during expiration from the pulmonary trunk to the segmental pulmonary arteries (P < 0.001) and for the inferior vena cava, the right atrium, and the ventricle. The incidence of nondiagnostic inspiratory studies ranged from 89 to 100%, depending on the observer. All studies were upgraded to fully acceptable diagnostic quality with follow-up expiratory imaging (P < 0.0001). Expiratory phase imaging was observed to have diagnostic impact in 78 to 88% of cases, with overall good to moderate interobserver agreement. In one case, pulmonary embolism was detected on the expiratory scan, which was not seen on the inspiratory scan. Expiratory imaging for nondiagnostic CTPA improves pulmonary arterial enhancement and improves diagnostic quality of CTPA by eliminating transient attenuation artifact, thus facilitating more accurate diagnosis and providing earlier treatment of pulmonary embolism.

Pitfalls of water distribution model skeletonization for surge analysis

Skeletonization is the process of representing a water distribution system model by only selected pipes. Skeletonized models normally are adequate for master planning and energy studies, but the degree of skeletonization that is acceptable for surge analysis is an often‐raised question. Most of the guidelines used for skeletonizing hydraulic network models do not apply for surge modeling. Replacing two or more pipes in parallel or series into an equivalent pipe with the same carrying capacity and trimming dead‐end mains can be readily applied for steady‐state analysis with virtually no effect on the resulting flows and pressures, but their effect on the system transient response can be significant. Moreover, the ratio of the pipe diameters greatly affects the transient pressure wave attenuation. In addition, dead ends, which may be caused by closure of check valves, lock pressure waves into the system in a cumulative fashion, and wave reflections will double both positive and negative pressures. The rules of skeletonization ignore the transient interaction of transient pressure waves in the different components and pipe properties of a water distribution system. In this article, case studies highlight the pitfalls of skeletonization in pressure surge analysis and support the conclusion that surge analysis requires a detailed model to accurately estimate transient pressure extremes in a water distribution system. A highly skeletonized model may overlook critical locations that are vulnerable for intrusion of potentially contaminated water.

Reduced HO-1 Protein Expression is Associated with More Severe Neurodegeneration after Transient Ischemia Induced by Cortical Compression in Diabetic Goto—Kakizaki Rats

Pronounced hyperglycemia provoked by extradural compression (EC) of the sensorimotor cortex was recently described in the non-insulin dependent Goto-Kakizaki (GK) diabetic rat. Compared with control Wistar rats, GK rats exhibited more extensive brain damage after cortical ischemia at 48 h of reperfusion (Moreira et al, 2007). We hypothesized that the enhanced brain injury in GK rats could be caused by differential regulation of the heme degrading enzyme heme oxygenase (HO)-1, known to interact with the expression of other target genes implicated in antioxidant defense, inflammation and neurodegeneration, such as superoxide dismutase (SOD)-1, -2, inducible nitric oxide synthase (iNOS), and tumor necrosis factor-alpha (TNFalpha). At 48 h after ischemia, relative mRNA expression of such target genes was compared between ipsilateral (compressed) and contralateral (uncompressed) hemispheres of GK rats, along with baseline comparison of sham, uncompressed GK and Wistar rats. Immunohistochemistry was performed to detect cellular and regional localization of HO-1 at this time point. Baseline expression of HO-1, iNOS, and TNFalpha mRNA was increased in the cortex of sham GK rats. GK rats showed pronounced hyperglycemia during EC and transient attenuation of regional cerebral blood flow recovery. At 48 h after reperfusion, HO-1 mRNA expression was 7- to 8-fold higher in the ischemic cortex of both strains, being the most upregulated gene under study. Heme oxygenase-1 protein expression was significantly reduced in diabetic rats and was found in perilesional astrocytes and rare microglial cells, in both strains. The reduced HO-1 protein expression in GK rats at 48 h after reperfusion combined with more extensive neurodegeneration induced by EC, provides further in vivo evidence for a neuroprotective role of HO after brain ischemia.

Effects of Gamma Radiation on FcεRI and TLR-Mediated Mast Cell Activation

Ionizing gamma radiation has several therapeutic indications including bone marrow transplantation and tumor ablation. Among immune cells, susceptibility of lymphocytes to gamma radiation is well known. However, there is little information on the effects of gamma radiation on mast cells, which are important in both innate and acquired immunity. Previous studies have suggested that mast cells may release histamine in response to high doses of gamma radiation, whereas other reports suggest that mast cells are relatively radioresistant. No strong link has been established between gamma radiation and its effect on mast cell survival and activation. We examined both human and murine mast cell survival and activation, including mechanisms related to innate and acquired immune responses following gamma radiation. Data revealed that human and murine mast cells were resistant to gamma radiation-induced cytotoxicity and, importantly, that irradiation did not directly induce beta-hexosaminidase release. Instead, a transient attenuation of IgE-mediated beta-hexosaminidase release and cytokine production was observed which appeared to be the result of reactive oxygen species formation after irradiation. Mast cells retained the ability to phagocytose Escherichia coli particles and respond to TLR ligands as measured by cytokine production after irradiation. In vivo, there was no decrease in mast cell numbers in skin of irradiated mice. Additionally, mast cells retained the ability to respond to Ag in vivo as measured by passive cutaneous anaphylaxis in mice after irradiation. Mast cells are thus resistant to the cytotoxic effects and alterations in function after irradiation and, despite a transient inhibition, ultimately respond to innate and acquired immune activation signals.

CT and MRI study of transient hepatic attenuation difference

目的 分析短暂性肝密度异常(THAD)CT及MR表现,揭示THAD产生的原因,避免假阳性诊断和误诊.方法 回顾10例CT出现THAD的患者资料,5例MRI出现THAD的患者资料,均行平扫及动态增强.结果 7例CT出现一过性高灌注,4例MRI出现一过性高灌注;3例CT出现一过性低灌注,1例MRI出现一过性低灌注.结论 CT及MRI出现THAD,与CT及MRI较快速扫描有关,只有充分了解肝脏正常生理和病理情况下的血液供应特点,才能对可能出现的肝脏局部灌注异常作出正确的判断,结合平扫可以明确诊断。

Notch signalling becomes transiently attenuated during long-term memory consolidation in adult Wistar rats

Recent evidence has suggested a role for Notch in memory consolidation but the means by which this evolutionarily conserved mechanism serves these plasticity-related processes remains to be established. We have examined a role for this signalling pathway in the hippocampal dentate gyrus of Wistar rats at increasing times following passive avoidance conditioning. Our principal finding is that a transient attenuation of Notch signalling occurs at the 10–12 h post-training time. In this period, extracellular Notch-1 protein fragment exhibited a significant 2- to 3-fold increase but, by contrast, Notch-1 mRNA levels were significantly reduced. Moreover, transient inactivation of Notch-1 signalling was further suggested by concomitant reductions in the Notch ligand Jagged-1 and Notch-1 target protein Hes-1 mRNA levels. The C-terminal fragment of PS-1, necessary for γ-secretase activity, was also significantly reduced at the 12 h post-training time. These events were commensurate with the increase of a Notch immunoreactive fragment of 66 kDa in the nuclear fraction of the dentate gyrus. This fragment, identified with two different Notch-1 antisera, was not the expected NICD polypeptide of ∼110 kDa and its accumulation was found to correlate with a significantly reduced expression of the Hes-1 transcriptional repressor. During the period of reduced Notch activity, a transient increase in soluble β-catenin and GSK-3β phosphorylation was observed, indicating a reciprocal activation of the Wnt signalling pathway. As down-regulation of Notch signalling promotes differentiation and neurite outgrowth in post-mitotic neurons, it is proposed that this pathway regulates the integration of synapses transiently produced during memory consolidation.

Transient Hepatic Echogenicity Difference on Contrast-Enhanced Ultrasonography

The purpose of this study was to report and analyze a new contrast-enhanced ultrasonographic (CEUS) imaging finding, the transient hepatic echogenicity difference due to perfusion changes, using computed tomography (CT) as a reference standard. We retrospectively investigated the records of patients evaluated in a 2-year period, selecting those who had undergone both CT and CEUS within 15 days, who had CT evidence of a perfusion abnormality, and who had had a CEUS study that included the malperfused parenchymal area. There were 30 patients with 44 hepatic perfusion changes on CT scans (28 around liver focal lesions and 16 unrelated to focal lesions). Retrospectively, CEUS allowed recognition of 21 of 28 perifocal transient hepatic attenuation differences (THADs), 6 of 10 subsegmental THADs, 2 of 3 segmental THADs, and 1 of 3 lobar THADs. Only some of these abnormalities had been identified at the original CEUS examinations: 0 of 3 lobar THADs, 1 of 3 segmental THADs, 2 of 10 subsegmental THADs, and 16 of 28 perifocal THADs. Contrast-enhanced ultrasonography can show hepatic perfusion abnormalities similar to those well known from CT literature, although with a lower sensitivity. Knowledge of this transient hepatic echogenicity difference phenomenon may be relevant for avoiding incorrect image interpretation or incorrect tumor size measurement and for eventually identifying occult vascular disorders such as venous thrombosis or fistulas.

Rotor/active magnetic bearing transient control using wavelet predictive moderation

A novel method for predicting the ultimate steady-state vibration amplitudes from measured transient responses in multi-input, multi-output flexible rotor/magnetic bearing systems is presented. The technique is based around a multi-level wavelet coefficient analysis with in-built transient system dynamics. The relation between an input disturbance wavelet coefficient acting on the system and a measured vibration wavelet coefficient is identified theoretically for non-identical wavelets. A controller is formulated in the wavelet coefficient domain with control forces derived from proportional feedback of displacement wavelet coefficients. Improved transient performance is achieved using wavelet coefficient steady-state prediction to moderate the control signal. Experimental validation of the controller using mass-loss tests demonstrates the manner in which transient vibration attenuation may be achieved.

Transient Hepatic Intensity Differences: Part 1, Those Associated with Focal Lesions

The purpose of our study was to evaluate, on MRI, transient hepatic signal intensity differences (THID) that have already been seen on CT as transient hepatic attenuation differences (THAD) and to show the range of appearance of such arterial phenomena, when associated with focal lesions, in an effort to correlate morphology, cause, and pathogenesis. Hepatic arterial phenomena visualized on MRI should be known and recognized to avoid incorrect diagnoses and to improve the characterization of focal liver lesions because their shape can lead to an understanding of pathogenetic mechanisms.

Optimal vibration attenuation of an adhesively-bonded cantilevered single-lap joint

In this study the three-dimensional transient vibration attenuation of an adhesively-bonded cantilevered single-lap joint was controlled using actuators. First, the vibration attenuation of the adhesive joint, which was disturbed by applying a concentrated load to the free edge of the lower adherend, was determined without a control force. In order to reduce displacement level and vibration attenuation time, a variable transverse control force was applied to a point on the lower adherend surface using an actuator. The transient variation of the control force was expressed by a periodic function so that the damped vibration of the adhesive joint was decreased. The optimal transient variation of the control force applied by the actuator is an optimization problem requiring the minimization of the objective function including the total elastic strain and kinetic energies, and the actuator work. In addition, the optimum placement of the actuator on the surface of the lower adherend is the second optimization problem. Optimal transient control force history and optimal actuator position were determined using the Open Loop Control Approach and Genetic Algorithm. The peak displacement reduced by 69.6% and the attenuation time decreased by 33%. In addition, the control performance of two actuators was investigated. Thus, the first actuator was located at the optimal position of a single actuator case, and then the optimal transient variations of the control forces applied by both actuators and the optimal position of the second actuator were determined. An additional decrease of 30% in the total energy of the adhesive joint and in the total work of both actuators in comparison to the single actuator case was found, whereas the difference in the vibration attenuation time of the adhesive joint was minor.

Reversible attenuation of voltage of QRS complexes and P waves and shortening of QRS duration and QTc interval consequent to large perioperative intravenous fluid infusions

A 39-year-old woman with a gangrenous pyelonephritis and septic shock underwent a nephrectomy, in preparation for which, she received large preoperative fluid resuscitation. Quantitative evaluation of her serial standard electrocardiograms (ECGs) revealed reversible attenuation of voltage in association with peripheral edema (PERE), with the latter being eventually completely abolished. The transient low-voltage ECG (LVECG) (attenuated amplitudes of QRS complexes) was associated with parallel transient attenuation of the amplitude of P waves and shortening of the QRS duration and QTc, whereas the P-wave duration increased. Awareness of these ECG changes with PERE of varying pathophysiologic mechanisms is useful, ensuring avoidance of improper procedural and laboratory testing and correct measurement of wave amplitudes and ECG time intervals for proper ECG diagnosis. In addition, these ECG associations can be used as indices of the presence and course of PERE postoperatively, as well as in a large variety of medical settings.

Endoplasmic Reticulum Stress Induction of Insulin-like Growth Factor-binding Protein-1 Involves ATF4

Endoplasmic reticulum (ER) stress is sensed by cells in different physiopathological conditions in which there is an accumulation of unfolded proteins in the ER. A coordinated adaptive program called the unfolded protein response is triggered and includes translation inhibition, transcriptional activation of a set of genes encoding mostly intracellular proteins, and ultimately apoptosis. Here we show that insulin-like growth factor (IGF)-binding protein-1 (IGFBP-1), a secreted protein that modulates IGF bioavailability and has other IGF-independent effects, is potently induced during ER stress in human hepatocytes. Various ER stress-inducing agents were able to increase IGFBP-1 mRNA levels, as well as cellular and secreted IGFBP-1 protein up to 20-fold. A distal regulatory region of the human IGFBP-1 gene (-6682/-6384) containing an activating transcription factor 4 (ATF4) composite site was required for promoter activation upon ER stress. Mutation of the ATF4 composite site led to the loss of IGFBP-1 regulation. Electrophoretic mobility shift assay revealed an ER stress-inducible complex that was displaced by an ATF4 antibody. Knockdown of ATF4 expression using two specific small interfering RNAs impaired up-regulation of IGFBP-1 mRNA, which highlights the relevance of ATF4 in endogenous IGFBP-1 gene induction. In addition to intracellular proteins involved in secretory and metabolic pathways, we conclude that ER stress induces the synthesis of secreted proteins. Increased secretion of IGFBP-1 during hepatic ER stress may thus constitute a signal to modulate cell growth and metabolism and induce a systemic adaptive response.

Attenuation and impulse response for multiple scattering of light in atmospheric clouds and aerosols

Model phase functions for atmospheric clouds and aerosols typically comprise a narrow forward lobe (corona), a broad diffuse background, and a narrow backscattering peak (glory), which can reach relatively high values, especially for polyhedral scattering particles, such as hexagonal ice columns and plates. The influence of these three major components on the asymptotic and transient attenuation of the scattered light is compared for several analytic phase functions to assess the dependence of radiative transfer in clouds and aerosols on the choice of phase function. The impulse response (temporal evolution of the angular intensity distribution) is sensitive to the higher moments of the phase function and could prove to be a useful technique for inferring the optical scattering parameters of clouds and aerosols.

Endoplasmic Reticulum Stress Features Are Prominent in Alzheimer Disease but Not in Prion Diseases In Vivo

Prion diseases and Alzheimer disease (AD) share a variety of clinical and neuropathologic features (e.g. progressive dementia, accumulation of abnormally folded proteins in diseased tissue, and pronounced neuronal loss) as well as pathogenic mechanisms like generation of oxidative stress molecules and complement activation. Recently, it was suggested that neuronal death in AD may have its origin in the endoplasmic reticulum (ER). Cellular stress conditions can interfere with protein folding and subsequently cause accumulation of unfolded or misfolded proteins in the ER lumen. The ER responds to this by the activation of adaptive pathways, which are termed unfolded protein response (UPR). The UPR transducer PERK, which launches the most immediate response to ER stress (i.e. the transient attenuation of mRNA translation), and the downstream effector of PERK, eIF2alpha, were shown to be activated in AD. We demonstrate that neither in sporadic nor in infectiously acquired or inherited human prion diseases can the activated forms of PERK and eIF2alpha be detected, except when concomitant neurofibrillary pathology is present; whereas the distribution of phosphorylated PERK correlates with abnormally phosphorylated tau in AD. In brains of scrapie-affected mice and mice infected with sporadic or variant Creutzfeldt-Jakob disease, activated PERK is only very faintly expressed. The lack of prominent activation of the PERK-eIF2alpha pathway in prion diseases suggests that, in contrast to AD, ER stress does not play a crucial role in neuronal death in prion disorders.

Wavelet domain control of rotor vibration

This paper describes a novel application of the real-time wavelet transform in the control of rotor vibration. Vibration signal wavelet coefficients that relate to different time scales provide direct information on the system dynamic state, and can thus be used for feedback in a closed-loop control strategy that attenuates both transient and steady-state vibration components. Control force signals are synthesized from basis functions having a characteristic frequency and spacing interval closely matched to the rotational frequency. The control signal basis coefficients are generated by integral feedback of the wavelet coefficients such that under steady-state conditions the control forces eliminate measured rotor vibration. The controller synthesis problem is solved by iterative solution of a linear matrix inequality to obtain a gain matrix that satisfies H∞ norm-bound specifications for transient vibration attenuation. It is demonstrated experimentally that wavelet coefficients from multiple scale levels can be used in direct feedback to reduce levels of transient vibration caused by instantaneous changes in unbalance.