bluuebunny/crossref_metadata_2025 huggingface dataset:
Exhumation and metamorphism of an ultrahigh-grade terrane: geochronometric investigations of the Sudete Mountains (Bohemia), Poland and Czech Republic
Authors: Gordon S. M. , Schneider D. A. , Manecki M. , Holm D. K.
Published: August 2005

The Sudete Mountains, NE Bohemian Massif (Czech Republic and Poland), preserve abundant eclogitic and granulitic centimetre- to decimetre-scale boudins enveloped in a predominantly migmatitic matrix. Published geochronometry and thermobarometry from the UHP and UHT rocks broadly constrain the crystallization and initial stage 1 exhumation history for these units; however, the timing of stage 2 metamorphism and associated unroofing is less well constrained. New
in situ
ion microprobe Th–Pb monazite results, together with complementary U–Pb zircon and electron microprobe analyser total-Pb monazite results, on 11 amphibolite-facies gneissic to migmatitic samples, place important temporal constraints on the second stage of UHP and UHT metamorphism–exhumation. The Orlica–Snieznik Dome records UHP metamorphism occurring at 375 Ma and subsequent exhumation to midcrustal levels in supra-Barrovian conditions at
c
. 345–330 Ma. In contrast, the western Góry Sowie Block preserves evidence of HP-granulite conditions at
c
. 400 Ma, and exhumation to mid-crustal levels at 380–370 Ma, revealing a
c
. 30 million years difference in exhumation events between the neighbouring terranes. The eastern Góry Sowie Block preserves ages similar to the Orlica–Sneiznik Dome, suggesting that different preserved metamorphic–cooling histories are juxtaposed across the Sudetic Marginal fault. The bounding Niemcza shear zone yields preliminary Th–Pb dates that range from 380 ± 8 Ma to 283 ± 2 Ma, preserving a protracted metamorphic record that spans the exhumation history of the region. The distinct collapsed geochronologies of both terranes probably reflect rapid vertical transport of low-viscosity crust under supra-Barrovian conditions near the mid-crustal high-strength lid during oblique (transpressional) convergence.
The Functional Significance of Ribosomal (r)DNA Variation: Impacts on the Evolutionary Ecology of Organisms
Authors: Weider Lawrence J. , Elser James J. , Crease Teresa J. , Mateos Mariana , Cotner James B. , Markow Therese A.
Published: August 2005

▪ Abstract  The multi-gene family that encodes ribosomal RNA (the rDNA) has been the subject of numerous review articles examining its structure and function, as well as its use as a molecular systematic marker. The purpose of this review is to integrate information about structural and functional aspects of rDNA that impact the ecology and evolution of organisms. We examine current understanding of the impact of length heterogeneity and copy number in the rDNA on fitness and the evolutionary ecology of organisms. We also examine the role that elemental ratios (biological stoichiometry) play in mediating the impact of rDNA variation in natural populations and ecosystems. The body of work examined suggests that there are strong reciprocal feedbacks between rDNA and the ecology of all organisms, from microbes to metazoans, mediated through increased phosphorus demand in organisms with high rRNA content.
Current Pharmacotherapy for Alzheimer's Disease
Authors: Lleó A. , Greenberg S.M. , Growdon J.H.
Published: August 2005

Alzheimer's disease (AD) is an age-related neurodegenerative disease that affects approximately 4.5 million people in the United States. The mainstays of current pharmacotherapy for AD are compounds aimed at increasing the levels of acetylcholine in the brain, thereby facilitating cholinergic neurotransmission through inhibition of the cholinesterases. These drugs, known as acetylcholinesterase inhibitors (AChEIs), were first approved by the U.S. Food and Drug Administration (FDA) in 1995 based on clinical trials showing modest symptomatic benefit on cognitive, behavioral, and global measures. In 2004 the FDA approved memantine, an NMDA antagonist, for treating dementia symptoms in moderate to severe AD cases. In clinical practice, memantine may be co-administered with an AChEI, although neither drug individually or in combination affects the underlying pathophysiology of dementia. Dementia in AD results from progressive synaptic loss and neuronal death. As knowledge of the mechanisms responsible for neurodegeneration in AD increases, it is anticipated that neuroprotective drugs to slow or prevent neuronal dysfunction and death will be developed to complement current symptomatic treatments.
The Internet as Psychological Laboratory
Authors: Skitka Linda J. , Sargis Edward G.
Published: August 2005

▪ Abstract  This chapter reviews studies published in American Psychological Association (APA) journals from 2003–2004 and additional studies (received in response to listserv requests) that used the Internet to collect data (N=121 total studies). Specific examples of three kinds of Web-based research are reviewed: (a) translational (established methods and research questions are adapted to the Web), (b) phenomenological (behavior on the Web is the focus of study), and (c) novel (methodologically innovations unique to Web-based research). Among other findings, our review indicated that 21% of APA journals published at least one article that reported on Web-based research, most Web-based psychological research uses experimental methods, a surprising number use college student samples, and deception in Web-based research is not uncommon. Strengths and weaknesses of Web-based psychological research in general, and our sample of studies in particular, are reviewed with special attention to possible concerns about sampling and the use of deception.
T cell-induced inflammation of the small and large intestine in immunodeficient mice
Authors: Ostanin Dmitry V. , Pavlick Kevin P. , Bharwani Sulaiman , D′Souza Dwain , Furr Kathryn L. , Brown Carla M. , Grisham Matthew B.
Published: August 2005

It is well known that transfer of CD4+CD45RBhigh(naïve) T cells into syngeneic lymphocyte-deficient mice induces chronic colitis. However, no studies have reported the presence of small bowel inflammation in this T cell-dependent model. Therefore, the objective of this study was to evaluate and compare small and large bowel inflammation induced by transfer of naïve T cells into two different immunodeficient recipient mice. T and B cell-deficient recombinase activating gene 1-deficient [RAG knockout (KO)] and T cell-deficient T cell receptor-β × T cell receptor-δ double-deficient (TCR KO) mice were reconstituted with wild-type naïve T cells and observed for signs of disease. We found that reconstituted RAG KO mice developed moderate to severe colitis and inflammation of the entire small intestine at 6–8 wk after T cell transfer. Adoptive transfer of naïve T cells into TCR KO mice induced a milder form of chronic colitis and small bowel inflammation that was confined primarily to the duodenum at 10–12 wk after T cell transfer. T helper cell 1 and macrophage-derived proinflammatory cytokine mRNA levels correlated well with the localization and severity of the chronic large and small bowel inflammation. In addition, we observed comparable homing and expansion of donor lymphocytes in the gut and secondary lymphoid tissues of both recipients. Taken together, our data demonstrate that transfer of naïve T cells into immunodeficient recipient mice induces both chronic small and large bowel inflammation and that the presence of B cells in the TCR KO recipients may play a role in regulating chronic intestinal inflammation.
Nitric oxide inhibits gastric acid secretion by increasing intraparietal cell levels of cGMP in isolated human gastric glands
Authors: Berg Anna , Redéen Stefan , Grenegård Magnus , Ericson Ann-Charlott , Sjöstrand Sven Erik
Published: August 2005

We have previously identified cells containing the enzyme nitric oxide (NO) synthase (NOS) in the human gastric mucosa. Moreover, we have demonstrated that endogenous and exogenous NO has been shown to decrease histamine-stimulated acid secretion in isolated human gastric glands. The present investigation aimed to further determine whether this action of NO was mediated by the activation of guanylyl cyclase (GC) and subsequent production of cGMP. Isolated gastric glands were obtained after enzymatic digestion of biopsies taken from the oxyntic mucosa of healthy volunteers. Acid secretion was assessed by measuring [14C]aminopyrine accumulation, and the concentration of cGMP was determined by radioimmunoassay. In addition, immunohistochemistry was used to examine the localization of cGMP in mucosal preparations after stimulation with the NO donor S-nitroso- N-acetylpenicillamine (SNAP). SNAP (0.1 mM) was shown to decrease acid secretion stimulated by histamine (50 μM); this effect was accompanied by an increase in cGMP production, which was histologically localized to parietal cells. The membrane-permeable cGMP analog dibuturyl-cGMP (db-cGMP; 0.1–1 mM) dose dependently inhibited acid secretion. Additionally, the effect of SNAP was prevented by preincubating the glands with the GC inhibitor 4 H-8-bromo-1,2,4-oxadiazolo[3,4-d]benz[b][1,4]oxazin-1-one (10 μM). We therefore suggest that NO in the human gastric mucosa is of physiological importance in regulating acid secretion. Furthermore, the results show that NO-induced inhibition of gastric acid secretion is a cGMP-dependent mechanism in the parietal cell involving the activation of GC.
Mechanical stretch-induced serotonin release from pulmonary neuroendocrine cells: implications for lung development
Authors: Pan Jie , Copland Ian , Post Martin , Yeger Herman , Cutz Ernest
Published: August 2005

Pulmonary neuroendocrine cells (PNEC) produce amine (serotonin, 5-HT) and peptides (e.g., bombesin, calcitonin) with growth factor-like properties and are thought to play an important role in lung development. Because physical forces are essential for lung growth and development, we investigated the effects of mechanical strain on 5-HT release in PNEC freshly isolated from rabbit fetal lung and in the PNEC-related tumor H727 cell line. Cultures exposed to sinusoidal cyclic stretch showed a significant 5-HT release inhibitable with gadolinium chloride (10 nM), a blocker of mechanosensitive channels. In contrast to hypoxia (Po2 ∼ 20 mmHg), stretch-induced 5-HT release was not affected by Ca2+-free medium or nifedipine (50 μM), excluding the exocytic pathway. In H727 cells, stretch failed to release calcitonin, a peptide stored within dense core vesicles (DCV), whereas hypoxia caused massive calcitonin release. 5-HT released by mechanical stretch is derived predominantly from the cytoplasmic pool, because it is rapid (∼5 min) and is releasable from early (20 days of gestation) fetal PNEC containing few DCV. Both mechanical stretch and hypoxia upregulated expression of tryptophan hydroxylase, the rate-limiting enzyme of 5-HT synthesis. We conclude that mechanical strain is an important physiological stimulus for the release of 5-HT from PNEC via mechanosensitive channels with potential effects on lung development and resorption of lung fluid at the time of birth.
Unusual small supernumerary marker chromosome (sSMC) 9 in a Klinefelter patient
Authors: Liehr T. , Mrasek K. , Starke H. , Claussen U. , Schreiber G.
Published: August 2005

Small supernumerary marker chromosomes (sSMC) are small additional chromosomes characterizable for their origin only by molecular cytogenetic approaches. sSMC have been reported previously in four types of syndromes associated with chromosomal imbalances: in ∼150 cases with Turner syndrome, 26 cases with Down syndrome and only one case each with Klinefelter syndrome and “Triple-X”-syndrome. Here we report the second case with an sSMC detected in addition to a Klinefelter karyotype. Molecular cytogenetics applying centromere-specific multicolor FISH (cenM-FISH) and a specific subcentromere-specific (subcenM-FISH) probe set characterized the sSMC as a dic(9)(:p12→q11.1::q11.1→ p11.1:). The reported patient was described with hypogonadism, gynaecomastia plus a bronchial carcinoma. The patient’s clinical features are discussed in connection with other Klinefelter cases and possible consequences of presence of the sSMC(9). Furthermore, a suggestion is made for the mode of sSMC-formation in this case.
A common ancestral glycoprotein (GP) 9 1828A>G (Asn45Ser) gene mutation occurring in European families from Australia and Northern Europe with Bernard-Soulier syndrome (BSS)
Authors: Morel-Kopp Marie-Christine , Clemetson Jeannine M. , Clemetson Kenneth J. , Kekomaki Riitta , Kroll Hartmut , Michaelides Katerina , Tuddenham Edward G. D. , Vanhoorelbeke Karen , Ward Christopher M. , Helena Liang Hai Po
Published: August 2005

Bernard-Soulier syndrome (BSS) is an extremely rare hereditary bleeding disorder, caused by mutations occurring in the Glycoprotein (GP) Ibα, GPIbβ and GP9 genes that encode for the corresponding subunits of platelet GPIb-V-IX adhesion receptor complex. BSS has been reported in many populations, mostly behaving in an autosomal-recessive manner. While the great majority of BSS mutations are unique to a single individual or family, the GP9 1828A>G Asn45Ser mutation, which we have identified in an undocumented Australian Caucasian, has already been reported in multiple unrelated Caucasian families from various Northern and Central European countries. Haplotype analysis of 19 BSS patients from 15 unrelated Northern European families (including 2 compound heterozygote siblings from a British family previously published, and 17 1828A>G Asn45Ser homozygotes), showed that 14 of these BSS patients from 11 of the 1828A>G Asn45Ser homozygote families share a common haplotype at the chromosomal region 3’ to the GP9 gene. Hence, the results suggest that the GP9 1828A>GAsn45Ser mutation in these families is ancient, and its frequent emergence in the European population is the result of a founder effect rather than recurrent mutational events. Association of the 1828A>G Asn45Ser mutation with variant haplotypes in 4 other Northern European BSS families raised the possibility of a second founder event, or rare recombinations in these families. Additional members from these ‘atypical’ lineages would need to be screened to resolve this question.
Advanced Glycosylation End Products Might Promote Atherosclerosis Through Inducing the Immune Maturation of Dendritic Cells
Authors: Ge Junbo , Jia Qingzhe , Liang Chun , Luo Yukun , Huang Dong , Sun Aijun , Wang Keqiang , Zou Yunzeng , Chen Haozhu
Published: August 2005

Objective—Both advanced glycosylation end products (AGEs) and dendritic cells (DCs) have been shown to play a causative role in atherosclerosis. However, whether they function interactively in the process remains uncertain. We therefore studied the effects of AGE–bovine serum albumin (AGE-BSA) on the maturation of DCs and the expressions of scavenger receptor-A (SR-A) and receptor for AGEs (RAGE) on DCs.

Methods and Results—AGE-BSA induced DCs maturation accompanied with increased expressions of CD1a, CD40, CD80, CD83, CD86, and MHC class II. The capacity of DCs to stimulate T-cell proliferation and secretion of cytokines (interferon [IFN], IFN-γ, interleukin [IL]-10 and IL-12) was also enhanced by AGE-BSA. AGE-BSA significantly upregulated SR-A and RAGE expression on DCs and the upregulation was abolished by inhibition of mitogen-activated protein (MAP) kinase Jnk, but not by that of Erk and p38 MAP kinase. AGE-BSA–induced expression of CD83 and secretion of IL-12 were partly inhibited by either an anti-RAGE neutralizing antibody or a Jnk inhibitor.

Conclusions—AGE-BSA induces maturation of DCs and augmented their capacity to stimulate T-cell proliferation and cytokine secretions possibly through upregulation of RAGE and SR-A, which at least in part through Jnk. These findings might explain in part the interactive roles of AGEs and DCs in the processes of atherosclerosis.
Assessment of Hemostatic Risk Factors in Predicting Arterial Thrombotic Events
Authors: Feinbloom David , Bauer Kenneth A.
Published: August 2005

Arterial thrombosis results from endovascular injury and, to a lesser extent, alterations in hemostatic equilibrium. Although multiple hereditary and acquired hemostatic risk factors have been described in the pathophysiology of venous thrombosis, the degree and type of abnormalities that contribute to arterial thrombosis are less well understood. Endothelial cell injury with the elaboration of proinflammatory mediators stimulates the process of arterial thrombosis. Although this is most often the result of endovascular injury attributable to atherosclerotic disease, other disease states can elicit a similar response as well. Similarly, once thrombosis has been initiated, variations in the activity of coagulation proteins and endogenous anticoagulants, as well as the kinetics of platelet aggregation, may alter the effectiveness of thrombus formation. Epidemiological studies have identified several acquired or inherited states that may result in endothelial damage or altered hemostatic equilibrium, thereby predisposing patients to arterial thrombosis. These include hyperhomocysteinemia, elevated C-reactive protein, antiphospholipid antibodies, elevated fibrinogen, Factor VII, plasminogen activator inhibitor-1 (PAI-1), hereditary thrombophilias, and platelet hyper-reactivity. This review explores our present understanding of these risk factors in the development of arterial thrombotic events. At present, the literature supports a role for hyperhomocysteinemia, elevated C-reactive protein, and elevated fibrinogen as risk factors for arterial thrombosis. Similarly, the literature suggests that lupus anticoagulants and, to a lesser extent, elevated titers of cardiolipin IgG antibodies predispose to arterial vascular events. In certain subsets of patients, including those with concomitant cardiac risk factors, <55 years of age, and women, hereditary thrombophilias such as carriership of the factor V Leiden and the prothrombin G20210A mutations may confer a higher risk of arterial thrombosis. However, the data on Factor VII, PAI-1, and platelet receptor polymorphisms are contradictory or lacking.
Cardiac-Specific Loss of N-Cadherin Leads to Alteration in Connexins With Conduction Slowing and Arrhythmogenesis
Authors: Li Jifen , Patel Vickas V. , Kostetskii Igor , Xiong Yanming , Chu Antony F. , Jacobson Jason T. , Yu Cindy , Morley Gregory E. , Molkentin Jeffery D. , Radice Glenn L.
Published: August 2005

The remodeling of ventricular gap junctions, as defined by changes in size, distribution, or function, is a prominent feature of diseased myocardium. However, the regulation of assembly and maintenance of gap junctions remains poorly understood. To investigate N-cadherin function in the adult myocardium, we used a floxed N-cadherin gene in conjunction with a cardiac-specific tamoxifen-inducible Cre transgene. The mutant animals appeared active and healthy until their sudden death ≈2 months after deleting N-cadherin from the heart. Electrophysiologic analysis revealed abnormal conduction in the ventricles of mutant animals, including diminished QRS complex amplitude consistent with loss of electrical coupling in the myocardium. A significant decrease in the gap junction proteins, connexin-43 and connexin-40, was observed in N-cadherin–depleted myocytes. Perturbation of connexin function resulted in decreased ventricular conduction velocity, as determined by optical mapping. Our data suggest that perturbation of the N-cadherin/catenin complex in heart disease may be an underlying cause, leading to the establishment of the arrythmogenic substrate by destabilizing gap junctions at the cell surface.
Expression and Phosphorylation of the Na-Pump Regulatory Subunit Phospholemman in Heart Failure
Authors: Bossuyt Julie , Ai Xun , Moorman J. Randall , Pogwizd Steven M. , Bers Donald M.
Published: August 2005

Intracellular [Na] is ≈3 mmol/L higher in heart failure (HF; in our arrhythmogenic rabbit model;

3

), and this can profoundly affect cardiac Ca and contractile function via Na/Ca exchange and Na/H exchange. Na/K-ATPase is the primary mechanism of Na extrusion. We examine here in HF rabbits (and human hearts) expression of Na/K-ATPase isoforms and phospholemman (PLM), a putative Na/K-ATPase regulatory subunit that inhibits pump function and is a major cardiac phosphorylation target. Na/K-ATPase α1- and α2-isoforms were reduced in HF in rabbit ventricular homogenates (by 24%) and isolated myocytes (by 30% and 17%), whereas α3 was increased (50%) in homogenates and decreased (52%) in myocytes (
P
<0.05). Homogenate Na/K-ATPase activity in left ventricle was also decreased in HF. However, we showed previously that Na/K-ATPase characteristics in intact ventricular myocytes were unaltered in HF. To reconcile these findings, we assessed PLM expression, phosphorylation, and association with Na/K-ATPase. PLM coimmunoprecipitated with Na/K-ATPase α1 and α2 in control and HF rabbit myocytes. PLM expression was reduced in HF by 42% in isolated rabbit left ventricular (LV) myocytes, by 48% in rabbit LV homogenates, and by 24% in human LV homogenate. The fraction of PLM phosphorylated at Ser-68 was increased dramatically in HF. Our results are consistent with a role for PLM analogous to that of phospholamban for SR Ca-ATPase (SERCA): inhibition of Na/K-ATPase function that is relieved on PLM phosphorylation. So reduced Na/K-ATPase expression in HF may be functionally offset by lower inhibition by PLM (because of reduced PLM expression and higher PLM phosphorylation).
Heme Oxygenase-1 Is Expressed in Carotid Atherosclerotic Plaques Infected by
Helicobacter pylori
and Is More Prevalent in Asymptomatic Subjects
Authors: Ameriso Sebastian F. , Villamil Agustina Ruiz , Zedda Christine , Parodi Juan C. , Garrido Sergio , Sarchi María Inés , Schultz Marcelo , Boczkowski Jorge , Sevlever Gustavo E.
Published: August 2005

Background and Purpose—

It is not well established what are the features, if any, that distinguish symptomatic from asymptomatic carotid atherosclerotic plaques. Inducible heme oxygenase-1 (HO-1) is a component of cellular defense mechanisms against oxidative stress. We aimed to assess the presence of
Helicobacter pylori (H pylori
) and the expression of HO-1 in carotid atherosclerotic plaques of patients with and without prior neurologic symptoms attributable to the operated artery.

Methods—

We examined 25 symptomatic and 23 asymptomatic carotid atherosclerotic plaques removed during endarterectomy and 7 normal carotid arteries obtained at autopsy. We investigated the presence of
H pylori
DNA in the vessel wall and performed immunohistochemical detection of HO-1.

Results—

H pylori
DNA was present in 28 plaques and HO-1 was expressed in 30 plaques. HO-1 was found in 27
H pylori-
positive specimens but in only 3
H pylori-
negative specimens (
P
<0.001). All 7 normal carotid arteries were negative for both
H pylori
and HO-1. Although 82% of asymptomatic specimens were positive for
H pylori
and 87% for HO-1, only 36% of symptomatic specimens were positive for both
H pylori
and HO-1 (
P
<0.01).

Conclusions—

This study suggests a strong association between
H pylori
infection and expression of HO-1 in carotid atherosclerotic plaques. There was a substantial prevalence of these features in specimens obtained from asymptomatic subjects.
Social Interaction Improves Experimental Stroke Outcome
Authors: Craft Tara K.S. , Glasper Erica R. , McCullough Louise , Zhang Ning , Sugo Nobuo , Otsuka Takashi , Hurn Patricia D. , DeVries A. Courtney
Published: August 2005

Background and Purpose—

Social interaction can have a profound effect on health. The purpose of the present study was to determine whether affiliative social interactions before and after stroke improve ischemic outcomes as assessed through histological analysis and behavioral assays.

Methods—

Male and female C57BL/6 mice were housed individually or with an ovariectomized female. Behavioral assessments were made 24 hours before 60 or 90 minutes of transient intraluminal middle cerebral artery occlusion (MCAO) or SHAM surgery and after 7 days of reperfusion. Two hours after behavioral testing on day 7, infarct size was determined by 2,3,5-triphenyltetrazolium histology, and blood samples were collected for assessment of corticosterone and C-reactive protein (CRP) concentrations.

Results—

Pair housing significantly decreased infarct size and improved contralateral paw use in 60-minute MCAO males and 90-minute MCAO females compared with socially isolated cohorts. Housing condition had no significant effect on infarct size in females that underwent 60 minutes of MCAO, but pair housing was associated with improved contralateral paw use relative to socially isolated mice. In a separate cohort of males, intraischemic CRP concentration was significantly reduced in pair-housed males relative to isolated males.

Conclusions—

Affiliative interaction during the peri-ischemic period reduces intraischemic CRP concentration, decreases ischemic damage in male and female mice, and improves behavioral outcome.
Leukocyte Count Predicts Microembolic Doppler Signals During Carotid Stenting
Authors: Aronow Herbert D. , Shishehbor Mehdi , Davis DonaLee A. , Katzan Irene L. , Bhatt Deepak L. , Bajzer Christopher T. , Abou-Chebl Alex , Derk Krieger W. , Whitlow Patrick L. , Yadav Jay S.
Published: August 2005

Background and Purpose—

Protected stenting has emerged as a safe and effective alternative to endarterectomy for the treatment of carotid stenosis in patients at high operative risk. Distal microembolization occurs invariably during carotid stenting. Little is known about the relationship between systemic inflammation and embolization during carotid stenting.

Methods—

We examined 43 consecutive patients who underwent carotid stenting with simultaneous transcranial Doppler (TCD) monitoring of the ipsilateral middle cerebral artery. Embolization was quantified by measuring microembolic signals (MES) on TCD. Preprocedure leukocyte counts were related to MES.

Results—

In unadjusted analyses, preprocedure leukocyte count was positively correlated with total procedural MES (
r
2
= 0.16;
P
=0.008). After considering age, gender, comorbidities, concomitant medical therapies, and the use of emboli prevention devices, increasing leukocyte count (β=35 for each 1000/μL increment;
P
=0.018) remained a significant and independent predictor of embolization (model-adjusted
r
2
=0.365;
P
=0.0005).

Conclusions—

Increasing preprocedure leukocyte count independently predicted more frequent MES during carotid stenting. These data suggest that systemic inflammation may influence the degree of procedural embolization.
The Linear Behavior of the System Middle Cerebral Artery Flow Velocity and Blood Pressure in Patients With Migraine
Authors: Müller Martin , Marziniak Martin
Published: August 2005

Background and Purpose—

Migraine is considered a disorder of the autonomic nervous system. We used the frequency analysis of dynamic cerebral autoregulation to assess whether blood flow regulation disturbances can be found at the frequencies at which sympathetic and parasympathetic activity is present.

Methods—

We measured simultaneously mean arterial blood pressure (BP) and the mean blood velocity (V) in the middle cerebral artery using transcranial Doppler ultrasound in 33 healthy controls (mean age±SD; 36±13 years) and in 22 patients with migraine (mean age; 39±7 years). Apart from assessing spectral power density for BP and V, we calculated the transfer function parameters gain, phase, and coherence at the frequency range between 0.0 and 0.25 Hz.

Results—

Compared with the controls, the spectral power density of BP and V exhibited a maximum magnitude of 10
26
in the migraine patients, whereas the maximum magnitude of BP and V in the controls was 10
−3
. Coherence showed no difference between patients and controls. Gain between BP and V increased in the controls >0.01 Hz but was ≈0 or negative in the migraine patients over the whole frequency range (
P
<0.01). The usually observed phase lead of V against BP was absent in the migraine patients in whom BP leaded V over nearly the whole frequency range (
P
<0.01).

Conclusions—

In terms of phase and gain, dynamic cerebral autoregulation is completely different in migraine patients compared with healthy subjects. Insofar, this can be interpreted as a lack of sympathetic and parasympathetic control of cerebral blood flow.
Association of Apolipoprotein E4 and Haplotypes of the Apolipoprotein E Gene With Lobar Intracerebral Hemorrhage
Authors: Woo Daniel , Kaushal Ritesh , Chakraborty Ranajit , Woo Jessica , Haverbusch Mary , Sekar Padmini , Kissela Brett , Pancioli Arthur , Jauch Edward , Kleindorfer Dawn , Flaherty Matthew , Schneider Alexander , Khatri Pooja , Sauerbeck Laura , Khoury Jane , Deka Ranjan , Broderick Joseph
Published: August 2005

Background and Purpose—

Conflicting reports in the literature exist with regard to the association of apolipoprotein E (apo E) alleles and lobar intracerebral hemorrhage (ICH). We genotyped 12 single-nucleotide polymorphisms in the 5′ upstream regulatory, exonic, and intronic regions of the apo E gene and performed genotype and haplotype association analyses.

Methods—

We prospectively enrolled subjects with hemorrhagic stroke and matched them with 2 controls based on age, race, and sex. Each case was reviewed by a physician to determine case status and location of the ICH. Multivariate logistic-regression modeling with backward elimination was used to determine significant risk factors for lobar ICH. Associations at the genotype and haplotype levels and linkage disequilibrium were conducted according to standard statistical methods.

Results—

Between May 1997 and December 2002, 315 cases of ICH were recruited, of whom 107 were lobar ICH cases matched to 205 controls. No association was found for apo E2, E3, or E4 with nonlobar ICH. Independent, significant risk factors for lobar ICH included apo E4, untreated hypertension, anticoagulant use, a first-degree relative with ICH, and ≤high school education (compared with >high school education). Treated hypercholesterolemia compared with “no history of hypercholesterolemia” was associated with a decreased risk of lobar ICH. Haplotype association analysis demonstrated a significant association of the apo E gene with lobar ICH among whites (
P
<0.0001) and blacks (
P
=0.0024).

Conclusions—

Apo E4 is independently associated with lobar ICH but not nonlobar ICH. Haplotypes of the apo E gene are associated with lobar ICH. Untreated hypertension is a risk factor for lobar ICH.
The Role of Wave Packets in Wave–Mean Flow Interactions during Southern Hemisphere Summer
Authors: Chang Edmund K. M.
Published: August 2005

In this study, reanalysis data produced by the European Centre for Medium-Range Weather Forecasts for 14 Southern Hemisphere (SH) summer seasons have been analyzed. All cases of hemispheric transient eddy kinetic energy (TEKE) maxima have been identified, and the evolution of the local energetics and planetary-scale flow anomalies accompanying these TEKE growth/decay episodes are composited.

The longitude–time evolution of the composite energetics shows the clear signature of a wave packet propagating eastward at a group velocity of about 27° longitude per day and undergoing a life cycle of growth and decay, with the energetics within a volume close to the wave packet center dominating the hemispheric mean energetics. When individual cases are examined, 52% are found to resemble the composite and have the energetics life cycle dominated by the evolution of a single wave packet, and an additional 21% are found to be dominated by the evolution of two wave packets having similar amplitudes. Only the remaining 27% can be regarded as having experienced TEKE growth and decay throughout much of the hemisphere.

The zonal mean flow and eddy feedback anomalies (i.e., reduction in the meridional temperature gradient due to the effects of the eddy heat fluxes, as well as increase in the barotropic shear due to a narrowing of the midlatitude jet through the effects of the eddy momentum fluxes) associated with the cases dominated by the evolution of a single wave packet are also found to be dominated by anomalies close to the wave packet center.

The fact that hemispheric wave growth/decay is often dominated by the evolution of a single wave packet has interesting dynamical consequences when the climatological basic flow is not zonally symmetric. When a wave packet propagates over regions of enhanced baroclinicity, it can extract more energy from the mean flow via baroclinic conversion, leading to its preferential growth. On the other hand, when a wave packet propagates over regions of weak baroclinicity, baroclinic conversion is suppressed; hence any packet growth must be due to other processes. By examining the location of wave packet peaks when hemispheric TEKE is at a maximum, it is observed that hemispheric mean TEKE peaks much more frequently when the dominant wave packet is located downstream of the region with strongest baroclinicity. In addition, the growth in TEKE for these cases is usually dominated by an increase in baroclinic conversion. In contrast, for the small number of cases in which the hemispheric mean TEKE maximum occurs when the dominant wave packet is located downstream of the region with weakest baroclinicity, the growth of the hemispheric TEKE is instead dominated by a reduction in barotropic dissipation.
QT and QTc Interval With Standard and Supratherapeutic Doses of Darifenacin, a Muscarinic M3 Selective Receptor Antagonist for the Treatment of Overactive Bladder
Authors: Serra Denise B. , Affrime Melton B. , Bedigian Martin P. , Greig Gerard , Milosavljev Slavica , Skerjanec Andrej , Wang Yibin
Published: August 2005

Prolongation of QT interval on an electrocardiogram is a valuable predictor of a drug's ability to cause potentially fatal ventricular tachyarrhythmia (torsades de pointes). Darifenacin is a muscarinic M3 selective receptor antagonist developed for the treatment of overactive bladder, a debilitating condition that is particularly prevalent in the older population. This 7‐day, randomized, parallel‐group study (n = 188) measured QT/QTc interval in healthy volunteers receiving once‐daily darifenacin at steady‐state therapeutic (15 mg) and supratherapeutic (75 mg) doses, alongside controls receiving placebo or moxifloxacin (positive control, 400 mg) once daily. There was no significant increase in QTcF interval with darifenacin treatment compared with placebo. Mean changes from baseline at pharmacokinetic Tmax versus placebo were −0.4 and −2.2 milliseconds in the darifenacin 15 mg and 75 mg groups, respectively, compared with +11.6 milliseconds in the moxifloxacin group (P <.01). This study demonstrates that darifenacin does not prolong QT/QTc interval.
Symptom Prevalence and Treatments Among Mexican Americans With Type 2 Diabetes
Authors: García Alexandra A.
Published: August 2005

Purpose

The purpose of this study was to examine the prevalence of diabetes-related symptoms among Mexican Americans with type 2 diabetes, their perceptions of symptom seriousness, treatments used to self-manage the symptoms, and ratings of treatment effectiveness.

Methods

As part of a larger descriptive correlational study conducted with 87 Mexican American adults in a southwest metropolitan area, data were collected during one-on-one interviews during outpatient visits using the Diabetes Symptom Self-care Inventory and analyzed with descriptive methods, t tests, and χ2s.

Results

Participants experienced 4.9 diabetes-related symptoms in a 30-day period and used a variety of treatments to self-manage the symptoms. Many of the self-management strategies were not appropriate for the most common causes of the symptoms. Few people tested their blood glucose levels in response to symptoms even though most owned glucometers.

Conclusions

Most people who experience diabetes symptoms used self-care to treat the symptoms, did not verify the cause of the symptom, and perceived their treatments as effective. The appropriateness of the treatments used cannot be evaluated without knowing the etiology of the symptom for a particular person and time. Clinicians must assess symptoms and their treatments to best develop effective individualized treatments.
Disordered Eating Behaviors in Youth With Type 1 Diabetes
Authors: Kelly Sarah Dion , Howe Carol J. , Hendler Jennifer Paige , Lipman Terri H.
Published: August 2005

Eating disorders are a significant health problem for many adolescents and are described as occurring along a spectrum of symptoms including disordered eating behaviors and clinical eating disorders. Poor self-esteem and body image, intense fear of gaining weight or refusal to maintain weight, and purging unwanted calories are clinical features of some eating disorders. Type 1 diabetes is a chronic illness with marked insulin deficiency. Chronic hyperglycemia creates a state of glucosuria with subsequent weight loss. Diabetes treatment focuses on intensive daily management of blood glucose by balancing insulin, food intake, and physical activity. Insulin omission offers an easy method for the purging of unwanted calories. The combination of these 2 illnesses is potentially deadly and also leads to an increased risk of poor diabetes outcomes. This includes poor metabolic control (measured by elevated hemoglobin A1C), increased risk of diabetic ketoacidosis, and microvascular complications such as retinopathy and nephropathy. Diabetes clinicians should be aware of the potential warning signs in an adolescent with diabetes as well as assessment and treatment options for eating disorders with concomitant type 1 diabetes. This article reviews the available data on the prevalence, screening tools, assessment guidelines, and treatment options for eating disorders in youth with type 1 diabetes.
Anatomical Acromioclavicular Ligament Reconstruction
Authors: Grutter Paul W. , Petersen Steve A.
Published: August 2005

Background

Current surgical treatments for acromioclavicular separations do not re-create the anatomy of the acromioclavicular joint.

Hypothesis

Anatomical acromioclavicular reconstruction re-creates the strength of the native acromioclavicular joint and is stronger than a modified Weaver-Dunn repair.

Study Design

Controlled laboratory study.

Methods

The native acromioclavicular joint in 6 fresh-frozen cadaveric upper extremities was stressed to failure under uniaxial tension in the coronal plane. A modified Weaver-Dunn procedure, anatomical acromioclavicular reconstruction using a palmaris longus graft, and anatomical acromioclavicular reconstruction using a flexor carpi radialis graft were then performed sequentially. Each repair was stressed to failure. Load-displacement curves and mechanism of failure were recorded for each.

Results

Loads at failure for the native acromioclavicular joint complex, modified Weaver-Dunn procedure, anatomical acromioclavicular reconstruction using a palmaris longus tendon graft, and anatomical acromioclavicular reconstruction using a flexor carpi radialis tendon graft were 815 N, 483 N, 326 N, and 774 N, respectively. The strength of the native acromioclavicular joint complex was significantly different from the modified Weaver-Dunn repair (P <. 001) and the anatomical acromioclavicular reconstruction using a palmaris longus tendon graft (P <. 001) but not from the anatomical acromioclavicular reconstruction using a flexor carpi radialis tendon graft (P =. 607).

Conclusion

The strength of the described anatomical acromioclavicular reconstruction is limited by the tendon graft used. Anatomical acromioclavicular reconstruction with a flexor carpi radialis tendon graft re-creates the tensile strength of the native acromioclavicular joint complex and is superior to a modified Weaver-Dunn repair.
The Diagnostic Value of Cerebrospinal Fluid Tau Protein in Dementing and Nondementing Neuropsychiatric Disorders
Authors: Paraskevas George P. , Kapaki Elisabeth , Liappas Ioannis , Theotoka Ioulia , Mamali Ioanna , Zournas Christos , Lykouras Lefteris
Published: August 2005

Cerebrospinal fluid (CSF) total tau protein (τT) is increased in Alzheimer’s disease (AD) and may be of some help in the diagnostic work-up of demented patients. The aim of the present study was to investigate the diagnostic aid and the additional help (over that of clinical criteria) of τT in different clinical situations. Double-sandwich enzyme-linked immunosorbent assay was used to quantify τT in 61 healthy controls and 241 patients with various neuropsychiatric diseases. Our results suggest that CSF τT offers significant additional information over that of clinical criteria of AD, for the discrimination of AD from normal aging, depression, synucleinopathy, and possibly vascular dementia. However, for the differential diagnosis from frontotemporal dementia, corticobasal ganglionic degeneration, and secondary dementia, the diagnostic value is inadequate.
Women's Role Expectations and Identity Development in India
Authors: Dhawan Nisha
Published: August 2005

Women's education, employment, and family roles and the interrelations between them have attracted increasing attention during the last few years. Feminists have dispelled long held notions about “women's place” and the accepted myths about their nature and function (Goldstien, 1972). Over the last few decades there has been a tremendous change in laws, attitudes, and norms affecting women's status, roles, and development in society in India. As a result of which women have ventured beyond the traditional role of wife and mother, and have sought employment and careers outside the home, and have actively participated in the economic and social development of the nation (Liddle & Joshi, 1986). There is a restructuring and reorientation of women's roles in contemporary society. However, not much empirical knowledge is available about these changes and the impact they have on women's behaviour, values, or attitudes and identities (Johnson, 1992). Rapid social changes in women's career and family roles are accompanied by a significant transition in their attitude towards career and family. Research in the last decade highlighted the complex relationships between a woman's objective roles and her subjective attitudes regarding these roles, which affect her overall life satisfaction and sense of identity in society (Phillips & Imhoff, 1997). This study examines the role expectation and satisfaction, fears, dreams, aspirations, sense of competence, or lack of it, among college women in contemporary Indian society.
Sustainable Forestry in Sweden: The Effect of Competition Among Private Certification Schemes
Authors: Gulbrandsen Lars H.
Published: August 2005

Comparing the practice of two certification schemes in Swedish forestry, the Forest Stewardship Council (FSC) and a forest owner-dominated competitor, the author explores the capacity of forest certification to ameliorate environmental degradation in forestry while attending to different stakeholder interests. Although the inclusiveness and stringency of the FSC might impede its ability to attend to industry needs, it has a greater capacity than the forest owner-dominated scheme to enhance environmental protection in forestry. Second, although competition for support and rule-making authority has resulted in convergence of the two schemes, the forest owner-dominated program has not adopted decision-making rules and structures to reduce the influence of forest owners in standard development and operation. Third, effective implementation of non-state forest governance schemes requires national forest law enforcement and well-functioning government administrations. This helps explain why forest certification initiatives have been more successful in Sweden and other developed countries than in developing countries.
The Forest Stewardship Council: Risk and Potential of Private Forest Governance
Authors: Pattberg Philipp H.
Published: August 2005

Among the many organizations active in the forestry sector, the Forest Stewardship Council is claimed to be one of the most effective, in terms of its effect on forestry and the political discourse. This article takes the first decade of private forest politics as a starting point for an assessment of the advantages and disadvantages of private systems of rules operating on the transnational level. It points to four open questions: (a) the problem of uneven geographic representation and the resulting disadvantages for developing countries; (b) the question of long-term financial support for private politics; (c) the problem of competing schemes and the resulting contradictory signals toward consumers and policy makers; and (d) generic structural limitations to market-based governance. These empirical observations, derived from analyzing one prominent private system, are generalized to a wider set of private systems of rules operating at the global level to assess the future of private governance in sustainability politics.
The Role of the Safety Net in Employer Health Benefit Decisions
Authors: Marquis M. Susan
Published: August 2005

The potential for sizable crowd-out of private expenditures by public insurance and delivery programs has been demonstrated. However, there is limited evidence about whether this stems from decisions of employers about their health benefit package or by decisions of workers. This study focuses on the role of public programs on employer decisions to offer insurance and the amount the employer contributes to the premium, using data from a large survey of employers and a database describing community characteristics. The study finds that both public insurance and public delivery programs have a significant effect on employer decisions, but the magnitude of the effect is small. Policies to limit crowd-out should focus on incentives to make continued private insurance purchase attractive to workers rather than incentives to employers.
VA-Medicare Dual Beneficiaries’ Enrollment in Medicare HMOs: Access to VA, Availability of HMOs, and Favorable Selection
Authors: Shen Yujing , Hendricks Ann , Li Duozhe , Gardner John , Kazis Lewis
Published: August 2005

This study examined the association between Veterans Administration (VA)-Medicare dual beneficiaries’ HMO enrollment and factors including sociodemographics, access/attachment to VA, self-reported health status, and characteristics of Medicare HMO markets. The results showed that availability of Medicare HMOs and less access to VA care were the major predictors of VA-Medicare dual beneficiaries’ HMO enrollment. Other significant predictors of HMO enrollment were age (65-69), having no college education, VA priority status (low income; less than 50 percent service disability). There was some evidence of favorable selection measured by self-reported health status. The identified HMO enrollment profile can position VA better in attracting and managing the care of these beneficiaries and in meeting potentially large shifts in their need for VA care if Medicare benefits or policies change markedly.
Apoptosis: A Basic Physiologic Process in Wound Healing
Authors: Rai Nirendra K. , Tripathi Kamlakar , Sharma Deborshi , Shukla Vijay K.
Published: August 2005

Apoptosis, or programmed cell death, is a complex network of biochemical pathways for controlling such events in a cell. Apoptosis is essential, as its failure can lead to disease. Because apoptosis concerns the regulation of sequential events, including the removal of inflammatory cells and the evolution of granulation tissue into scar tissue, it has an essential role in wound repair. This article examines the literature and proposes that apoptosis features in the development of diabetic foot wounds. Hyperglycemia deregulates the sequential apoptotic events by multiple mechanisms, leading to delayed wound healing. Deregulated apoptosis is emerging as a prominent cause of delayed wound healing, especially in diabetic wounds, along with the well-known triad of peripheral vascular disease, neuropathy, and infection.