bluuebunny/crossref_metadata_2025 huggingface dataset:
VIBRATIONAL SPECTRUM FOR THE LINEAR LATTICE CHAIN GAINED BY VIRTUE OF THE "INVARIANT EIGEN-OPERATOR" METHOD
Authors: FAN HONG-YI , WU HAO , XU XUE-FEN
Published: October 2005

We propose an operator Hamiltonian (a ring of identically coupled harmonic oscillators) to describe the linear lattice chain with Born–von Karmann boundary condition. We apply the method of "invariant eigen-operator" to study this Hamiltonian and derive its invariant eigen-operator. The vibrational spectrum is thus obtained. This approach seems concise and direct and can be extended to tackle other Hamiltonian models.
THE RANGE OF EXCHANGE INTERACTIONS AND CURIE TEMPERATURE IN La0.67-xBixCa0.33MnO3 COMPOUNDS
Authors: GENCER H. , ATALAY S.
Published: October 2005

Magnetic properties of Bi 3+-doped La 0.67-x Bi x Ca 0.33 MnO 3(x = 0, 0.05, 0.1, 0.2) are investigated. Using the mean-field and ferromagnetic spin-wave theory at low temperatures, total exchange integrals and Curie temperatures are calculated in the range 0≤x≤0.2. Calculated values of Tc are in good agreement with those obtained by magnetic measurements. In addition, the total exchange integral decrease with Bi 3+ shows the existence of canted ferromagnetic order in the samples, as observed in experimental results.
CURRENT INDUCED LOCAL SPIN POLARIZATION DUE TO THE SPIN-ORBIT COUPLING IN A TWO DIMENSIONAL NARROW STRIP
Authors: WANG QIAN , SHENG LI
Published: October 2005

The current induced local spin polarization due to weak Rashba spin-orbit coupling in narrow strip is studied. In the presence of longitudinal charge current, local spin polarizations appear in the sample. The spin polarization perpendicular to the plane has opposite sign near the two edges. The in-plane spin polarization in the direction perpendicular to the sample edges also appears, but does not change sign across the sample. From our scaling analysis based on increasing the strip width, the out-of-plane spin polarization is important mainly in a system of mesoscopic size, and thus appears not to be associated with the spin-Hall effect in bulk samples.
Electroacupuncture at ST-36 accelerates colonic motility and transit in freely moving conscious rats
Authors: Iwa Masahiro , Matsushima Megumi , Nakade Yukiomi , Pappas Theodore N. , Fujimiya Mineko , Takahashi Toku
Published: October 2005

Acupuncture is useful for functional bowel diseases, such as constipation and diarrhea. However, the mechanisms of beneficial effects of acupuncture on colonic function have scarcely ever been investigated. We tested the hypothesis that electroacupuncture (EA) at ST-36 stimulates colonic motility and transit via a parasympathetic pathway in conscious rats. Hook-shaped needles were inserted at bilateral ST-36 (lower limb) or BL-21 (back) and electrically stimulated at 10 Hz for 20 min. We also studied c-Fos expression in response to EA at ST-36 in Barrington's nucleus of the pons. EA at ST-36, but not BL-21, significantly increased the amplitude of motility at the distal colon. The calculated motility index of the distal colon increased to132 ± 9.9% of basal levels ( n = 14, P < 0.05). In contrast, EA at ST-36 had no stimulatory effects in the proximal colon. EA at ST-36 significantly accelerated colonic transit [geometric center (GC) = 6.76 ± 0.42, n = 9, P < 0.001] compared with EA at BL-21 (GC = 5.23 ± 0.39, n = 7). The stimulatory effect of EA at ST-36 on colonic motility and transit was abolished by pretreatment with atropine. EA-induced acceleration of colonic transit was also abolished by extrinsic nerve denervation of the distal colon (GC = 4.69 ± 0.33, n = 6). The number of c-Fos-immunopositive cells at Barrington's nucleus significantly increased in response to EA at ST-36 to 8.1 ± 1.1 cells/section compared with that of controls (2.4 ± 0.5 cells/section, n = 3, P < 0.01). It is concluded that EA at ST-36 stimulates distal colonic motility and accelerates colonic transit via a sacral parasympathetic efferent pathway (pelvic nerve). Barrington's nucleus plays an important role in mediating EA-induced distal colonic motility in conscious rats.
Relationship between 5-aminoimidazole-4-carboxamide-ribotide and AMP-activated protein kinase activity in the perfused mouse heart
Authors: Zhang Li , Frederich Markus , He Huamei , Balschi James A.
Published: October 2005

AMP-activated protein kinase (AMPK) is a cellular energy sensor whose activity responds to AMP concentration ([AMP]). An agent that activates AMPK in cells is 5-aminoimidazole-4-carboxamide-1-riboside (AICA-riboside). Phosphorylated AICA-riboside or AICA-ribotide (ZMP) is an AMP analog. It is generally assumed that ZMP accumulation does not alter [AMP]. Additionally, the effect of AICA-riboside on AMPK activity of the heart is uncertain. Two hypotheses were tested in the isolated mouse heart: 1) sufficient ZMP concentration ([ZMP]) forms to increase AMPK activity, and 2) [ZMP] accumulation increases [AMP]. Perfusion of isolated mouse hearts with Krebs-Henseleit buffer containing 0.15–2 mM AICA-riboside concentration resulted in [ZMP] of 2–8 mM. ZMP accumulation reduced phosphocreatine concentration, which increased cytosolic [AMP]. In hearts with [ZMP] less than ∼3 mM, in vivo AMPK allosteric activity effects of ZMP were observed; AMPK phosphorylation and [AMP] were not increased. With [ZMP] between 3 and 5 mM, in vitro AMPK activity and phosphorylation increased with unchanged [AMP]. This occurred in hearts perfused with 0.25 mM AICA-riboside for 48 min and 0.5 mM AICA-riboside for 24 min. The [ZMP] resulting in 50% AMPK activity (covalent phosphorylation of AMPK) was 4.1 ± 0.6 mM. Hearts with [ZMP] >5 mM displayed increased [AMP] and AMPK activity that was not different from hearts with similar [AMP] with no [ZMP]; the half-maximal activity of AMP was 5.6 ± 1.6 μM. Thus, in mouse hearts, AICA-riboside was metabolized to [ZMP] adequately to increase AMPK activity. Higher [ZMP] also increased cytosolic [AMP], which affects AMPK activity.
Epoxyeicosatrienoic and dihydroxyeicosatrienoic acids dilate human coronary arterioles via BKCachannels: implications for soluble epoxide hydrolase inhibition
Authors: Larsen Brandon T. , Miura Hiroto , Hatoum Ossama A. , Campbell William B. , Hammock Bruce D. , Zeldin Darryl C. , Falck John R. , Gutterman David D.
Published: October 2005

Epoxyeicosatrienoic acids (EETs) are metabolized by soluble epoxide hydrolase (sEH) to form dihydroxyeicosatrienoic acids (DHETs) and are putative endothelium-derived hyperpolarizing factors (EDHFs). EDHFs modulate microvascular tone; however, the chemical identity of EDHF in the human coronary microcirculation is not known. We examined the capacity of EETs, DHETs, and sEH inhibition to affect vasomotor tone in isolated human coronary arterioles (HCAs). HCAs from right atrial appendages were prepared for videomicroscopy and immunohistochemistry. In vessels preconstricted with endothelin-1, three EET regioisomers (8,9-, 11,12-, and 14,15-EET) each induced a concentration-dependent dilation that was sensitive to blockade of large-conductance Ca2+-activated K+(BKCa) channels by iberiotoxin. EET-induced dilation was not altered by endothelial denudation. 8,9-, 11,12-, and 14,15-DHET also dilated HCA via activation of BKCachannels. Dilation was less with 8,9- and 14,15-DHET but was similar with 11,12-DHET, compared with the corresponding EETs. Immunohistochemistry revealed prominent expression of cytochrome P-450 (CYP450) 2C8, 2C9, and 2J2, enzymes that may produce EETs, as well as sEH, in HCA. Inhibition of sEH by 1-cyclohexyl-3-dodecylurea (CDU) enhanced dilation caused by 14,15-EET but reduced dilation observed with 11,12-EET. DHET production from exogenous EETs was reduced in vessels pretreated with CDU compared with control, as measured by liquid chromatography electrospray-ionization mass spectrometry. In conclusion, EETs and DHETs dilate HCA by activating BKCachannels, supporting a role for EETs/DHETs as EDHFs in the human heart. CYP450s and sEH may be endogenous sources of these compounds, and sEH inhibition has the potential to alter myocardial perfusion, depending on which EETs are produced endogenously.
P2 antagonist PPADS attenuates responses of thin fiber afferents to static contraction and tendon stretch
Authors: Kindig Angela E. , Hayes Shawn G. , Hanna Ramy L. , Kaufman Marc P.
Published: October 2005

Injection into the arterial supply of skeletal muscle of pyridoxal phosphate-6-azophenyl-2′,4′-disulfonic acid (PPADS), a P2 receptor antagonist, has been shown previously to attenuate the reflex pressor responses to both static contraction and to tendon stretch. In decerebrated cats, we tested the hypothesis that PPADS attenuated the responses of groups III and IV muscle afferents to static contraction as well as to tendon stretch. We found that injection of PPADS (10 mg/kg) into the popliteal artery attenuated the responses of both group III ( n = 16 cats) and group IV afferents ( n = 14 cats) to static contraction. Specifically, static contraction before PPADS injection increased the discharge rate of the group III afferents from 0.1 ± 0.05 to 1.6 ± 0.5 impulses/s, whereas contraction after PPADS injection increased the discharge of the group III afferents from 0.2 ± 0.1 to only 1.0 ± 0.5 impulses/s ( P < 0.05). Likewise, static contraction before PPADS injection increased the discharge rate of the group IV afferents from 0.3 ± 0.1 to 1.0 ± 0.3 impulses/s, whereas contraction after PPADS injection increased the discharge of the group IV afferents from 0.2 ± 0.1 to only 0.3 ± 0.1 impulses/s ( P < 0.05). In addition, PPADS significantly attenuated the responses of group III afferents to tendon stretch but had no effect on the responses of group IV afferents. Our findings suggest that both groups III and IV afferents are responsible for evoking the purinergic component of the exercise pressor reflex, whereas only group III afferents are responsible for evoking the purinergic component of the muscle mechanoreflex that is evoked by tendon stretch.
Vascular endothelial-derived semaphorin 3 inhibits sympathetic axon growth
Authors: Damon Deborah H.
Published: October 2005

Vascular sympathetic innervation is an important determinant of blood pressure and blood flow. The mechanisms that determine vascular sympathetic innervation are not well understood. Recent studies indicate that vascular endothelial cells (EC) express semaphorin 3A, a repulsive axon guidance cue. This suggests that EC would inhibit the growth of axons to blood vessels. The present study tests this hypothesis. RT-PCR and Western analyses confirmed that rat aortic vascular ECs expressed semaphorin 3A as well as other class 3 semaphorins (sema 3s). To determine the effects of EC-derived sema 3 on sympathetic axons, axon outgrowth was assessed in cultures of neonatal sympathetic ganglia grown for 72 h in the absence and presence of vascular EC. Nerve growth factor-induced axon growth in the presence of ECs was 50 ± 4% ( P < 0.05) of growth in the absence of ECs. ECs did not inhibit axon growth in the presence of an antibody that neutralized the activity of sema 3 ( P > 0.05). RT-PCR and Western analyses also indicated that sema 3s were expressed in ECs of intact arteries. To assess the function of sema 3s in arteries, sympathetic ganglia were grown in the presence of arteries for 72 h, and the percentage of axons that grew toward the artery was determined: 44 ± 4% of axons grew toward neonatal carotid arteries. Neutralization of sema 3s or removal of EC increased the percentage of axons that grew toward the artery (71 ± 8% and 72 ± 8%, respectively). These data indicate that vascular EC-derived sema 3s inhibit sympathetic axon growth and may thus be a determinant of vascular sympathetic innervation.
Inhaled nitric oxide induced NOS inhibition and rebound pulmonary hypertension: a role for superoxide and peroxynitrite in the intact lamb
Authors: Oishi Peter , Grobe Albert , Benavidez Eileen , Ovadia Boaz , Harmon Cynthia , Ross Gregory A. , Hendricks-Munoz Karen , Xu Jie , Black Stephen M. , Fineman Jeffrey R.
Published: October 2005

Previous in vivo studies indicate that inhaled nitric oxide (NO) decreases nitric oxide synthase (NOS) activity and that this decrease is associated with significant increases in pulmonary vascular resistance (PVR) upon the acute withdrawal of inhaled NO (rebound pulmonary hypertension). In vitro studies suggest that superoxide and peroxynitrite production during inhaled NO therapy may mediate these effects, but in vivo data are lacking. The objective of this study was to determine the role of superoxide in the decrease in NOS activity and rebound pulmonary hypertension associated with inhaled NO therapy in vivo. In control lambs, 24 h of inhaled NO (40 ppm) decreased NOS activity by 40% ( P < 0.05) and increased endothelin-1 levels by 64% ( P < 0.05). Withdrawal of NO resulted in an acute increase in PVR (60.7%, P < 0.05). Associated with these changes, superoxide and peroxynitrite levels increased more than twofold ( P < 0.05) following 24 h of inhaled NO therapy. However, in lambs treated with polyethylene glycol-conjugated superoxide dismutase (PEG-SOD) during inhaled NO therapy, there was no change in NOS activity, no increase in superoxide or peroxynitrite levels, and no increase in PVR upon the withdrawal of inhaled NO. In addition, endothelial NOS nitration was 18-fold higher ( P < 0.05) in control lambs than in PEG-SOD-treated lambs following 24 h of inhaled NO. These data suggest that superoxide and peroxynitrite participate in the decrease in NOS activity and rebound pulmonary hypertension associated with inhaled NO therapy. Reactive oxygen species scavenging may be a useful therapeutic strategy to ameliorate alterations in endogenous NO signaling during inhaled NO therapy.
Glutathione restores collagen degradation in TGF-β-treated fibroblasts by blocking plasminogen activator inhibitor-1 expression and activating plasminogen
Authors: Vayalil Praveen K. , Olman Mitchell , Murphy-Ullrich Joanne E. , Postlethwait Edward M. , Liu Rui-Ming
Published: October 2005

Transforming growth factor (TGF)-β plays an important role in tissue fibrogenesis. We previously demonstrated that reduced glutathione (GSH) supplementation blocked collagen accumulation induced by TGF-β in NIH-3T3 cells. In the present study, we show that supplementation of GSH restores the collagen degradation rate in TGF-β-treated NIH-3T3 cells. Restoration of collagen degradation by GSH is associated with a reduction of type I plasminogen activator inhibitor (PAI)-1 expression/activity as well as recovery of the activities of cell/extracellular matrix-associated tissue-type plasminogen activator and plasmin. Furthermore, we find that NIH-3T3 cells constitutively express plasminogen mRNA and possess plasmin activity. Blockade of cell surface binding of plasminogen/plasminogen activation with tranexamic acid (TXA) or inhibition of plasmin activity with aprotinin significantly reduces the basal level of collagen degradation both in the presence or absence of exogenous plasminogen. Most importantly, addition of TXA or active PAI-1 almost completely eliminates the restorative effects of GSH on collagen degradation in TGF-β treated cells. Together, our results suggest that the major mechanism by which GSH restores collagen degradation in TGF-β-treated cells is through blocking PAI-1 expression, leading to increased PA/plasmin activity and consequent proteolytic degradation of collagens. This study provides mechanistic evidence for GSH's putative therapeutic effect in the treatment of fibrotic disorders.
RNA interference for α-ENaC inhibits rat lung fluid absorption in vivo
Authors: Li Tianbo , Folkesson Hans G.
Published: October 2005

We used siRNA against the α-ENaC (epithelial Na channel) subunit to investigate ENaC involvement in lung fluid absorption in rats by the impermeable tracer technique during baseline and after β-adrenoceptor stimulation by terbutaline. Terbutaline stimulation of lung fluid absorption increased fluid absorption by 165% in pSi-0-pretreated rat lungs (irrelevant siRNA-generating plasmid). Terbutaline failed to increase lung fluid absorption in rats given the specific α-ENaC siRNA-generating plasmid (pSi-4). pSi-4 pretreatment reduced baseline lung fluid absorption by ∼30%. α-ENaC was undetectable in pSi-4-pretreated lungs, regardless of condition but was normal in pSi-0-pretreated lungs. We carried out a dose-response analysis where rats were given 0–200 μg/kg body wt pSi-4, and α-ENaC mRNA and protein expressions were analyzed. To reach IC50for α-ENaC mRNA expression, 32 μg/kg body wt pSi-4 was needed, and to reach IC50for α-ENaC protein expression, 59 μg/kg body wt pSi-4 was needed. We tested for lung tissue specificity and found no changes in β-ENaC expression, at either mRNA or protein level, as well as no changes in α1-Na-K-ATPase protein expression. We isolated alveolar epithelial type II cells 24 h after in vivo pSi-4 pretreatment. In these cells, α-ENaC mRNA was undetectable, demonstrating that alveolar epithelial ENaC expression was attenuated after intratracheal α-ENaC siRNA-generating plasmid DNA instillation. We tested for organ specificity and found no changes in kidney α- and β-ENaC mRNA and protein expression. Thus we provide conclusive evidence that β-adrenoceptor stimulation of lung fluid absorption is critically ENaC dependent, whereas baseline lung fluid absorption seemed less ENaC dependent.
Partially adenosine deaminase-deficient mice develop pulmonary fibrosis in association with adenosine elevations
Authors: Chunn Janci L. , Mohsenin Amir , Young Hays W. J. , Lee Chun G. , Elias Jack A. , Kellems Rodney E. , Blackburn Michael R.
Published: October 2005

Adenosine, a signaling nucleoside, exhibits tissue-protective and tissue-destructive effects. Adenosine levels in tissues are controlled in part by the enzyme adenosine deaminase (ADA). ADA-deficient mice accumulate adenosine levels in multiple tissues, including the lung, where adenosine contributes to the development of pulmonary inflammation and chronic airway remodeling. The present study describes the development of pulmonary fibrosis in mice that have been genetically engineered to possess partial ADA enzyme activity and, thus, accumulate adenosine over a prolonged period of time. These partially ADA-deficient mice live for up to 5 mo and die from apparent respiratory distress. Detailed investigations of the lung histopathology of partially ADA-deficient mice revealed progressive pulmonary fibrosis marked by an increase in the number of pulmonary myofibroblasts and an increase in collagen deposition. In addition, in regions of the distal airways that did not exhibit fibrosis, an increase in the number of large foamy macrophages and a substantial enlargement of the alveolar air spaces suggest emphysemic changes. Furthermore, important proinflammatory and profibrotic signaling pathways, including IL-13 and transforming growth factor-β1, were activated. Increases in tissue fibrosis were also seen in the liver and kidneys of these mice. These changes occurred in association with pronounced elevations of lung adenosine concentrations and alterations in lung adenosine receptor levels, supporting the hypothesis that elevation of endogenous adenosine is a proinflammatory and profibrotic signal in this model.
GEF-H1 is involved in agonist-induced human pulmonary endothelial barrier dysfunction
Authors: Birukova Anna A. , Adyshev Djanybek , Gorshkov Boris , Bokoch Gary M. , Birukov Konstantin G. , Verin Alexander D.
Published: October 2005

Endothelial cell (EC) permeability is precisely controlled by cytoskeletal elements [actin filaments, microtubules (MT), intermediate filaments] and cell contact protein complexes (focal adhesions, adherens junctions, tight junctions). We have recently shown that the edemagenic agonist thrombin caused partial MT disassembly, which was linked to activation of small GTPase Rho, Rho-mediated actin remodeling, cell contraction, and dysfunction of lung EC barrier. GEF-H1 is an MT-associated Rho-specific guanosine nucleotide (GDP/GTP) exchange factor, which in MT-unbound state stimulates Rho activity. In this study we tested hypothesis that GEF-H1 may be a key molecule involved in Rho activation, myosin light chain phosphorylation, actin remodeling, and EC barrier dysfunction associated with partial MT disassembly. Our results show that depletion of GEF-H1 or expression of dominant negative GEF-H1 mutant significantly attenuated permeability increase, actin stress fiber formation, and increased MLC and MYPT1 phosphorylation induced by thrombin or MT-depolymerizing agent nocodazole. In contrast, expression of wild-type or activated GEF-H1 mutants dramatically enhanced thrombin and nocodazole effects on stress fiber formation and cell retraction. These results show a critical role for the GEF-H1 in the Rho activation caused by MT disassembly and suggest GEF-H1 as a key molecule involved in cross talk between MT and actin cytoskeleton in agonist-induced Rho-dependent EC barrier regulation.
Inhibition of phosphodiesterase 4 amplifies cytokine-dependent induction of arginase in macrophages
Authors: Erdely Aaron , Kepka-Lenhart Diane , Clark Melissa , Zeidler-Erdely Patti , Poljakovic Mirjana , Calhoun William J. , Morris Sidney M.
Published: October 2005

Arginase is greatly elevated in asthma and is thought to play a role in the pathophysiology of this disease. As inhibitors of phosphodiesterase 4 (PDE4), the predominant PDE in macrophages, elevate cAMP levels and reduce inflammation, they have been proposed for use in treatment of asthma and chronic obstructive pulmonary disease. As cAMP is an inducer of arginase, we tested the hypothesis that a PDE4 inhibitor would enhance macrophage arginase induction by key cytokines implicated in asthma and other pulmonary diseases. RAW 264.7 cells were stimulated with IL-4 or transforming growth factor (TGF)-β, with and without the PDE4 inhibitor rolipram. IL-4 and TGF-β increased arginase activity 16- and 5-fold, respectively. Rolipram alone had no effect but when combined with IL-4 and TGF-β synergistically enhanced arginase activity by an additional 15- and 5-fold, respectively. The increases in arginase I protein and mRNA levels mirrored increases in arginase activity. Induction of arginase II mRNA was also enhanced by rolipram but to a much lesser extent than arginase I. Unlike its effect in RAW 264.7 cells, IL-4 alone did not increase arginase activity in human alveolar macrophages (AM) from healthy volunteers. However, combining IL-4 with agents to induce cAMP levels induced arginase activity in human AM significantly above the level obtained with cAMP-inducing agents alone. In conclusion, agents that elevate cAMP significantly enhance induction of arginase by cytokines. Therefore, consequences of increased arginase expression should be evaluated whenever PDE inhibitors are proposed for treatment of inflammatory disorders in which IL-4 and/or TGF-β predominate.
Multiple Toll-like receptor ligands induce an IL-6 transcriptional response in skeletal myocytes
Authors: Frost Robert A. , Nystrom Gerald J. , Lang Charles H.
Published: October 2005

Toll-like receptors (TLRs) comprise a critical sentinel that monitors body compartments for the presence of pathogens. Skeletal muscle expresses TLRs and responds to pathogen-associated molecular patterns (PAMPs), such as lipopolysaccharide (LPS), by mounting an innate immune response. In the present study, we used C2C12myocytes as a model system for skeletal muscle during infection. C2C12cells responded to LPS in a time frame and with a pattern of gene expression that faithfully mimicked the response of skeletal muscle to LPS in vivo. LPS from a variety of Escherichia coli serotypes stimulated IL-6 synthesis. C2C12cells expressed TLR1–7, but not TLR8 or TLR9, mRNA by RT-PCR. A synthetic tripalmitoylated cysteine-, serine-, and lysine-containing peptide (Pam) and LPS from Porphyromonas gingivalis, two TLR2 ligands, also stimulated IL-6 expression. LPS and Pam stimulated luciferase activity driven from NF-κB and IL-6 promoter-containing plasmids, and this response was blunted when the NF-κB binding site was mutated. LPS- and Pam-stimulated IL-6 expression was inhibited by the proteasome inhibitor MG-132 and the IκB kinase-2 (IKK2) inhibitor 2-[(aminocarbonyl)amino]-5-(4-fluorophenyl)-3-thiophenecarboxamide (TPCA-1). Pam-stimulated NF-κB and IL-6 promoter activities were disrupted by a dominant-negative form of TLR2, but not TLR4. Local injection of LPS or Pam into the gastrocnemius muscle stimulated IL-6 mRNA expression in the injected, but not the contralateral, muscle. The LPS- but not Pam-stimulated expression of IL-6 mRNA was blunted in skeletal muscle of mice carrying an inactivating mutation in TLR4. The data suggest that skeletal muscle and muscle cells recognize pathogen-associated molecules with specific TLRs to initiate an IL-6 transcriptional response.
Segment-specific resistivity improves body fluid volume estimates from bioimpedance spectroscopy in hemodialysis patients
Authors: Zhu F. , Kuhlmann M. K. , Kaysen G. A. , Sarkar S. , Kaitwatcharachai C. , Khilnani R. , Stevens L. , Leonard E. F. , Wang J. , Heymsfield S. , Levin N. W.
Published: October 2005

Discrepancies in body fluid estimates between segmental bioimpedance spectroscopy (SBIS) and gold-standard methods may be due to the use of a uniform value of tissue resistivity to compute extracellular fluid volume (ECV) and intracellular fluid volume (ICV). Discrepancies may also arise from the exclusion of fluid volumes of hands, feet, neck, and head from measurements due to electrode positions. The aim of this study was to define the specific resistivity of various body segments and to use those values for computation of ECV and ICV along with a correction for unmeasured fluid volumes. Twenty-nine maintenance hemodialysis patients (16 men) underwent body composition analysis including whole body MRI, whole body potassium (40K) content, deuterium, and sodium bromide dilution, and segmental and wrist-to-ankle bioimpedance spectroscopy, all performed on the same day before a hemodialysis. Segment-specific resistivity was determined from segmental fat-free mass (FFM; by MRI), hydration status of FFM (by deuterium and sodium bromide), tissue resistance (by SBIS), and segment length. Segmental FFM was higher and extracellular hydration of FFM was lower in men compared with women. Segment-specific resistivity values for arm, trunk, and leg all differed from the uniform resistivity used in traditional SBIS algorithms. Estimates for whole body ECV, ICV, and total body water from SBIS using segmental instead of uniform resistivity values and after adjustment for unmeasured fluid volumes of the body did not differ significantly from gold-standard measures. The uniform tissue resistivity values used in traditional SBIS algorithms result in underestimation of ECV, ICV, and total body water. Use of segmental resistivity values combined with adjustment for body volumes that are neglected by traditional SBIS technique significantly improves estimations of body fluid volume in hemodialysis patients.
Superior Vena Cava Anomalies in the Generation of Angina Pectoris
Authors: Hindupur Sandeep , Lammoglia Francisco J.
Published: October 2005

Superior vena cava anomalies are rare occurrences caused by variations in the development of the embryonic venous system. Persistent left superior vena cavae are the most common congenital aberrations in the thoracic venous system, with an incidence of 0.3–0.5%, but their association in the absence of a right superior vena cava is extremely rare and scarcely reported. We report two case studies describing persistent left superior vena cavae found with and without a right superior vena cava in patients presenting with chest pain. A discussion regarding superior vena cava abnormalities as well as the etiology, associations, and diagnosis of these unusual entities follows.
Electrocardiographic Abnormalities in Patients with Right Ventricular Dilation due to Acute Pulmonary Embolism
Authors: Sukhija Rishi , Aronow Wilbert S. , Ahn Chul , Kakar Priyanka
Published: October 2005

In a study of 190 patients with acute pulmonary embolism, right ventricular dilation was present in 64 (34%), mean age 58 ± 15 years. The 18 electrocardiographic abnormalities on the 12-lead electrocardiogram had a sensitivity of 8–69%, a specificity of 70–98%, a positive predictive value of 23–69%, a negative predictive value of 64–83%, a likelihood ratio for a positive test of 1.3–4.4, and a likelihood ratio for a negative test of 0.41–1.10 in predicting right ventricular dilation in patients with acute pulmonary embolism.
Clinical and Neuroimaging Correlates of Mild Cognitive Impairment in a Middle-Aged Community Sample: The Personality and Total Health through Life 60+ Study
Authors: Kumar Rajeev , Parslow Ruth A. , Jorm Anthony F. , Rosenman Stephen J. , Maller Jerome , Meslin Chantal , Anstey Kaarin J. , Christensen Helen , Sachdev Perminder S.
Published: October 2005

This cross-sectional study aimed at determining the clinical and structural brain magnetic resonance imaging correlates of mild cognitive impairment (MCI). The data presented here are from the first wave of the longitudinal Personality and Total Health through Life 60+ project. 2,551 community-dwelling individuals in the age range of 60–64 years were recruited randomly through the electoral roll. They were screened using Mini-Mental State Examination and a short cognitive battery. Those who screened positive underwent detailed medical and neuropsychological assessments. Of the 224 subjects who screened positive, 117 underwent a detailed assessment. Twenty-nine subjects fulfilled the Mayo Clinic criteria for MCI. Magnetic resonance imaging scans were analyzed for 26 subjects with MCI as well as normal controls. Subjects were clinically evaluated for depressive symptoms and major and minor depression syndromes. Logistic regression analysis was performed predicting MCI from anterior and mid-ventricular brain ratios, cortical atrophy measures, hippocampal volumes, volumes of amygdala and white matter hyperintensities after adjusting for age, gender, years of education, depression and physical disability. None of the neuroanatomical substrates appeared as predictors of MCI. The only predictors were higher depression scores and fewer years of education. Structural neuroimaging may not have an added advantage in the detection of MCI in middle-aged community-dwelling subjects. It may be that this age group is too young for such brain changes to be identified.
Significance of Vascular Endothelial Growth Factor Expression in Renal Tissue of Patients with Preeclamptic Nephropathy
Authors: Tang Zheng , Ren Hongqi , Yang Guang , Chen Huiping , Zhou Hong , Zeng Caihong , Liu Zhihong , Li Leishi
Published: October 2005

Objective: It was the aim of this study to evaluate the distribution and expression of vascular endothelial growth factor (VEGF) in kidneys of patients with preeclamptic nephropathy and their relationship with clinical and pathological manifestations. Methods: From May 1993 to August 2004, 19 patients with a mean age of 28.1 ± 4.53 years (range 23–40), diagnosed with preeclamptic nephropathy by renal biopsy, were enrolled in this study. Fifteen were nulliparous and 4 multipara. Their renal tissues were subjected to immunohistochemical staining by a four-layer peroxidase-antiperoxidase method using monoclonal anti-VEGF. Residual normal renal tissue obtained at nephrectomy served as control. The relationship between the expression pattern of VEGF and clinicopathological features was also investigated. Results: The expression of VEGF markedly increased in renal tissues of patients with preeclamptic nephropathy at the early stage of gestation termination in comparison with normal controls. However, over time, it gradually decreased and reached the level of normal controls (100 vs. 71.43 vs. 20%, p < 0.05). The degree of endothelial proliferation in the glomeruli was closely related to the expression of VEGF, which was stronger in patients with diffuse endothelial proliferation than in those with segment proliferation (p < 0.05). In addition, there was a proportional relationship between the expression of VEGF and the level of urinary protein excretion (p < 0.05). Conclusion: The patients with preeclamptic nephropathy showed strong expressions of VEGF in glomeruli, which were closely associated with glomerular endothelial lesions and proteinuria, and over time, gradually weakened to normal level after gestation termination.
Short-Term Secretory Regulation of Ghrelin during Growth Hormone Provocative Tests in Prepubertal Children with Various Growth Hormone Secretory Capacities
Authors: Matsuoka Hisafumi , Hosoda Hiroshi , Sugawara Hisae , Iwama Saika , Kim Hye Sook , Kangawa Kenji , Sugihara Shigetaka
Published: October 2005

Background and Objective: Ghrelin is a novel gastric peptide which stimulates GH secretion and has been demonstrated to have orexigenic and adipogenic properties. Insulin is a physiological and dynamic modulator of plasma ghrelin, and insulinemia possibly mediates the effect of the nutritional state on the plasma concentrations of ghrelin in adults. No data on the regulation of GH secretion by ghrelin have so far been reported, nor has the possible influence of hypoglycemia on the plasma ghrelin levels in children been reported. Methods: Provocative studies were performed using a variety of stimuli, including insulin-induced hypoglycemia, and glucagon, arginine and L-dopa loading. We studied a group of 27 children with short stature being investigated for GH deficiency (10 F, 17 M; age 4–14 years; height SDS –0.92 to –3.27); the subjects were instructed to fast overnight, and the following morning, the relationships among the plasma ghrelin, GH and glucose levels were investigated by determining the plasma ghrelin profiles during those provocative tests. Using a new method for determining the two types of ghrelin, samples were obtained for determination of the plasma ghrelin, serum glucose and serum GH levels after the administration of the aforementioned stimulating agents. Results: All the four stimuli caused a significant decrease in the circulating C- and N-ghrelin levels with a nadir at +30 min, with the exception of the N-ghrelin level following the L-dopa loading. During the same period, the plasma GH level increased following insulin, arginine and L-dopa loading, and the plasma glucose level increased significantly following glucagon loading. In the arginine and L-dopa load connected, a significant correlation was observed between the 30-min change in the serum GH level and the 30-min change in the plasma C-ghrelin level. In the multiple regression analysis to explain the 30-min change in the plasma level of C-ghrelin, the baseline plasma level of C-ghrelin (basal), height and % overweight were the only three significant parameters, accounting for 85.2% of the variance. Conclusion: This study demonstrated that the inverse relation between the circulating GH and ghrelin levels may indicate the existence of a feedback loop, and also lends support to the assumption of a GH-independent relationship between plasma ghrelin and glucose levels. These observations constitute further evidence to suggest that peripheral ghrelin is a direct growth-promoting hormone.
β-Catenin Overexpression Augments Angiogenesis and Skeletal Muscle Regeneration Through Dual Mechanism of Vascular Endothelial Growth Factor–Mediated Endothelial Cell Proliferation and Progenitor Cell Mobilization
Authors: Kim Kwang-il , Cho Hyun-Ju , Hahn Joo-Yong , Kim Tae-Youn , Park Kyung-Woo , Koo Bon-Kwon , Soo Shin Chan , Kim Cheol-Ho , Oh Byung-Heeh , Lee Myoung-Mook , Park Young-Bae , Kim Hyo-Soo
Published: October 2005

Objective—

β-Catenin plays a critical role in directing cell fate during embryogenesis, and uncontrollable activation leads to cancers, suggesting its importance in cell survival and proliferation. However, little is known regarding its role in endothelial cell (EC) and skeletal muscle proliferation and progenitor cell mobilization.

Methods and Results—

β-Catenin enhanced ECs proliferation, protected ECs from apoptosis, and increased the capillary forming capabilities, which was completely blocked by inhibition of its nuclear translocation. In addition, the increased proliferation by β-catenin was associated with increased expression of cyclin E2. In skeletal myocytes, β-catenin overexpression increased proliferation with cyclin D1 expression, decreased apoptosis, and induced hypertrophy. Furthermore, β-catenin induced the expression of vascular endothelial growth factor (VEGF) in skeletal myocytes, resulting in EC proliferation. In a mouse hindlimb ischemia model, β-catenin significantly increased recovery of blood perfusion, capillary density along with enhanced VEGF expression, and the number of proliferating ECs and myocytes. Local delivery of β-catenin also promoted angiogenic progenitor cell mobilization and increased the number of satellite cells.

Conclusions—

β-Catenin may be an important modulator of angiogenesis and myocyte regeneration not only by directly enhancing proliferation and survival of ECs and skeletal myocytes but also by inducing VEGF expression and promoting angiogenic progenitor cell mobilization and muscle progenitor cell activation.
Air Pollution and Hospital Admissions for Ischemic and Hemorrhagic Stroke Among Medicare Beneficiaries
Authors: Wellenius Gregory A. , Schwartz Joel , Mittleman Murray A.
Published: October 2005

Background and Purpose—

The association between short-term elevations in ambient air particles and increased cardiovascular morbidity and mortality is well documented. Ambient particles may similarly increase the risk of stroke.

Methods—

We evaluated the association between daily levels of respirable particulate matter (aerodynamic diameter ≤10 μm, PM
10
) and hospital admission for ischemic and hemorrhagic stroke among Medicare recipients (age ≥65 years) in 9 US cities using a 2-stage hierarchical model. In the first stage, we applied the time-stratified case-crossover design to estimate the effect of PM
10
in each city. We used a 3-day unconstrained, distributed lag model to simultaneously estimate the effect of PM
10
0 to 2 days before the admission day and controlled for meteorological covariates in all of the models. In the second stage, we used random-effects metaanalytic techniques to combine the city-specific effect estimates.

Results—

Ischemic (n=155 503) and hemorrhagic (19 314) stroke admissions were examined separately. For ischemic stroke, an interquartile range increase in PM
10
was associated with a 1.03% (95% CI, 0.04% to 2.04%) increase in admissions on the same day only. Similar results were observed with CO, NO
2
, and SO
2
. For hemorrhagic stroke, no association was observed with any pollutant 0 to 2 days before admission.

Conclusions—

These results suggest that elevations in ambient particles may transiently increase the risk of ischemic, but not hemorrhagic, stroke. Studies with more accurate assessment of timing of stroke onset are necessary to confirm or refute these findings.
Risk of Myocardial Infarction and Vascular Death After Transient Ischemic Attack and Ischemic Stroke
Authors: Touzé Emmanuel , Varenne Olivier , Chatellier Gilles , Peyrard Séverine , Rothwell Peter M. , Mas Jean-Louis
Published: October 2005

Background—

Whether stroke patients should be investigated for asymptomatic coronary artery disease remains matter of debate. Absolute risks of myocardial infarction (MI) and vascular death after a stroke have not been accurately assessed. We performed a systematic review and a meta-analysis to determine the risk of MI and nonstroke vascular death after transient ischemic attack (TIA) and ischemic stroke. Cohort studies of TIA or ischemic stroke patients were included if they were published between 1980 and March 2005, reported risk of MI and nonstroke vascular death, enrolled >100 patients, and had at least 1 year of follow-up. We included 39 studies in a total of 65 996 patients with mean follow-up of 3.5 years. Two reviewers independently carried out data extraction using a standardized form. Absolute annual risks were estimated through weighted meta-regressions with a random effect. To test the predictions of expected event rates derived from our analysis, we used individual patient data.

Summary of Review—

The annual risks were 2.1% (CI 95%: 1.9 to 2.4) for nonstroke vascular death, 2.2% (1.7 to 2.7) for total MI, 0.9% (0.7 to 1.2) for nonfatal MI and 1.1% (0.8 to 1.5) for fatal MI. The time course of risk was linear. Estimated risks fitted well with observed risks at the individual level. There was no heterogeneity in the absolute risks according to baseline study characteristics.

Conclusions—

Patients with TIA or stroke have a relatively high risk of MI and nonstroke vascular death. Additional research is needed to identify the determinants of coronary artery disease in stroke patients.
Phonotactic Knowledge and Lexical-Semantic Processing in One-year-olds: Brain Responses to Words and Nonsense Words in Picture Contexts
Authors: Friedrich Manuela , Friederici Angela D.
Published: October 2005

During their first year of life, infants not only acquire probabilistic knowledge about the phonetic, prosodic, and phonotactic organization of their native language, but also begin to establish first lexical-semantic representations. The present study investigated the sensitivity to phonotactic regularities and its impact on semantic processing in 1-year-olds. We applied the method of event-related brain potentials to 12-and 19-month-old children and to an adult control group. While looking at pictures of known objects, subjects listened to spoken nonsense words that were phonotactically legal (pseudowords) or had phonotactically illegal word onsets (nonwords), or to real words that were either congruous or incongruous to the picture contents. In 19-month-olds and in adults, incongruous words and pseudowords, but not non-words, elicited an N400 known to reflect mechanisms of semantic integration. For congruous words, the N400 was attenuated by semantic priming. In contrast, 12-month-olds did not show an N400 difference, neither between pseudo-and nonwords nor between incongruous and congruous words. Both 1-year-old groups and adults additionally displayed a lexical priming effect for congruous words, that is, a negativity starting around 100 msec after words onset. One-year-olds, moreover, displayed a phonotactic familiarity effect, that is, a widely distributed negativity starting around 250 msec in 19-month-olds but occurring later in 12-month-olds. The results imply that both lexical priming and phonotactic familiarity already affect the processing of acoustic stimuli in children at 12 months of age. In 19-month-olds, adult-like mechanisms of semantic integration are present in response to phonotactically legal, but not to phonotactically illegal, nonsense words, indicating that children at this age treat pseudo-words, but not nonwords, as potential word candidates.
When Blue is Larger than Red: Colors Influence Numerical Cognition in Synesthesia
Authors: Kadosh Roi Cohen , Sagiv Noam , Linden David E. J. , Robertson Lynn C. , Elinger Gali , Henik Avishai
Published: October 2005

In synesthesia, certain stimuli (“inducers”) may give rise to perceptual experience in additional modalities not normally associated with them (“concurrent”). For example, color-grapheme synesthetes automatically perceive achromatic numbers as colored (e.g., 7 is turquoise). Although synesthetes know when a given color matches the one evoked by a certain number, colors do not automatically give rise to any sort of number experience. The behavioral consequences of synesthesia have been documented using Stroop-like paradigms, usually using color judgments. Owing to the unidirectional nature of the synesthetic experience, little has been done to obtain performance measures that could indicate whether bidirectional cross-activation occurs in synesthesia. Here it is shown that colors do implicitly evoke numerical magnitudes in color-grapheme synesthetes, but not in nonsynesthetic participants. It is proposed that bidirectional co-activation of brain areas is responsible for the links between color and magnitude processing in color-grapheme synesthesia and that unidirectional models of synesthesia might have to be revised.
Dissociating Reading Processes on the Basis of Neuronal Interactions
Authors: Mechelli Andrea , Crinion Jennifer T. , Long Steven , Friston Karl J. , Ralph Matthew A. Lambon , Patterson Karalyn , McClelland James L. , Price Cathy J.
Published: October 2005

Previous studies of patients with phonological and surface alexia have demonstrated a double dissociation between the reading of pseudo words and words with atypical spelling-to-sound relationships. A corresponding double dissociation in the neuronal activation patterns for pseudo words and exception words has not, however, been consistently demonstrated in normal subjects. Motivated by the literature on acquired alexia, the present study contrasted pseudo words to exception words and explored how neuronal interactions within the reading system are influenced by word type. Functional magnetic resonance imaging was used to measure neuronal responses during reading in 22 healthy volunteers. The direct comparison of reading pseudo words and exception words revealed a double dissociation within the left frontal cortex. Pseudo words preferentially increased left dorsal premotor activation, whereas exception words preferentially increased left pars triangularis activation. Critically, these areas correspond to those previously associated with phonological and semantic processing, respectively. Word-type dependent interactions between brain areas were then investigated using dynamic causal modeling. This revealed that increased activation in the dorsal premotor cortex for pseudo words was associated with a selective increase in effective connectivity from the posterior fusiform gyrus. In contrast, increased activation in the pars triangularis for exception words was associated with a selective increase in effective connectivity from the anterior fusiform gyrus. The present investigation is the first to identify distinct neuronal mechanisms for semantic and phonological contributions to reading.
Delay-period Activity in the Prefrontal Cortex: One Function Is Sensory Gating
Authors: Postle Bradley R.
Published: October 2005

The prefrontal cortex (PFC) contributes to working memory functions via executive control processes that do not entail the storage, per se, of mnemonic representations. One of these control processes may be a sensory gating mechanism that facilitates retention of representations in working memory by down-regulating the gain of the sensory processing of intervening irrelevant stimuli. This idea was tested by scanning healthy young adults with functional magnetic resonance imaging while they performed a delayed face-recognition task. The 2 × 2 factorial design varied the factors of Memory (present, absent) and Distraction (present, absent). During memory-present trials, target and probe stimuli were individual gray-scale male faces. Memory-absent trials were identical, except that they employed the same recurring female faces (denoting a “no memory” trial). Distraction-present trials featured rapid serial visual presentation of bespectacled male faces during the two middle seconds of the delay. The first step of the analyses identified dorsolateral PFC (dlPFC) and inferior occipitotemporal cortex (IOTC) voxels exhibiting delay-period activity in memory-present/distraction-absent trials, that is, the “unfilled” delay. Within these voxels, distraction-evoked activity in the dlPFC was markedly higher during trials that required the concurrent short-term retention of information than on those that did not, whereas the opposite effect was seen in the IOTC. These results are consistent with the view that processes related to sensory gating account for a portion of the delay-period activity that is routinely observed in the dlPFC.