bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Ischemia‐Modified Albumin in Relation to Pacemaker and Defibrillator Implantation
Authors: SBAROUNI EFTIHIA , GEORGIADOU PANAGIOTA , PANAGIOTAKOS DEMOSTHENES , LIVANIS EFTHIMIOS , THEODORAKIS GEORGE N. , KREMASTINOS DIMITRIOS TH. 
Published: August 2010

Background: Ischemia‐modified albumin (IMA) is considered a marker of myocardial ischemia whereas cardiac enzymes are released when cardiac necrosis occurs. It has previously been shown that permanent pacemaker‐defibrillator insertion is associated with myocardial injury expressed as cardiac enzyme rise.
Objective: We assessed whether pacemaker‐defibrillator implantation also induces changes in IMA plasma levels and whether, therefore, myocardial ischemia precedes necrosis.
Methods: We studied 64 consecutive patients undergoing pacemaker or defibrillator implantation; 43 were men and 21 women and their age was 70 ± 11 years (range 23–84 years). Blood samples were collected at baseline, six hours and 48 hours following the procedure. IMA measured by the albumin cobalt binding test (ACB, Integra 800 analyzer), as well as creatine kinase (CK), the MB isoenzyme of creatine kinase (CK‐MB) and cardiac troponin I (Tn‐I) were evaluated.
Results: Data analysis showed that compared to baseline measurements, IMA increased at six hours (P = 0.015) and at 48 hours (P = 0.003)[97.6 ± 10.2 vs 101.4 ± 10.7 vs 102.1 ± 9.2 U/mL at baseline, six hours and 48 hours, respectively]; similarly, CK increased at six hours (P = 0.0001) and remained high at 48 hours (P = 0.0001) [74.9 ± 49.9 vs 136.1±186.7 vs 115.2 ± 63.9 mIU/mL], while CK‐MB increased at six hours (P = 0.0001), but returned to baseline values at 48 hours (P = 0.05) [0.90 ± 0.89 vs 1.27 ± 134 vs 0.71 ± 0.63 ng/mL] and Tn‐I increased at six hours (P = 0.0001) and returned to baseline levels at 48 hours (P = 0.32) [0.057 ± 0.23 vs 0.16 ± 0.36 vs 0.03 ± 0.045 ng/mL].
Conclusion: Permanent pacemaker‐defibrillator insertion is associated with myocardial ischemia and necrosis.
Electrophysiologic Characteristics of the Sinus Venosa in Patients with Typical Atrial Flutter
Authors: TAI CHING‐TAI , GERTRUDE ONG MARY , CHEN SHIH‐ANN 
Published: August 2010

Background: The sinus venosa is a posterior barrier of typical atrial flutter. However, its electrophysiology has not been studied.
Methods and Results: The study population included 20 patients with typical atrial flutter (Group 1) and 20 patients with paroxysmal supraventricular tachycardia (Group 2). The noncontact mapping system was used to evaluate the electrophysiology of the sinus venosa (SV) during coronary sinus (CS) and low right atrial (LRA) pacing and atrial activation during typical atrial flutter. The results showed 12 of Group 1 patients (60%) had two lines of block, one in the CT and the other in the SV. The virtual electrograms in the CT and SV showed double potentials. Eight patients (40%) had only one line of block in the CT. During atrial pacing at the cycle length of 500 ms, nine of Group 1 patients had a line of block on the SV. None of the Group 2 patients had a line of block. During atrial pacing at the CL of 300 ms, 12 of Group 1 patients had a line of block on the SV. Eight of Group 1 patients had transverse conduction through the SV during atrial pacing. None of the Group 2 had a line of block.
Conclusions: This study showed that the SV formed the posterior line of block in 60% of the patients with typical atrial flutter. Fixed conduction block and rate‐dependent conduction block in the SV may be involved in the pathogenesis of typical AFL.
Comparison of Two Strategies to Reduce Ventricular Pacing in Pacemaker Patients
Authors: PÜRERFELLNER HELMUT , BRANDT JOHAN , ISRAEL CARSTEN , SHELDON TODD , JOHNSON JAMES , TSCHELIESSNIGG KARLHEINZ , SPERZEL JOHANNES , BORIANI GIUSEPPE , PUGLISI ANDREA , MILASINOVIC GORAN 
Published: August 2010

Background:

Managed Ventricular Pacing (MVP) and Search AV+ (SAV+) are two pacing algorithms designed to reduce ventricular pacing. MVP promotes conduction by operating in AAI/R mode with backup ventricular pacing during atrioventricular block (AVB). SAV+ operates in DDD/R mode with a nominal AV extension of 290 ms during atrial sensing and 320 ms during atrial pacing. The reduction in ventricular pacing was compared with these two algorithms in pacemaker patients.
Methods:

The EnRhythm and EnPulse clinical studies assessed the percentage of ventricular pacing (%VP) after 1 month. Each patient's AVB status was assigned using the following hierarchical categories: persistent third‐degree AVB (p3AVB), episodic third‐degree AVB (e3AVB), second‐degree AVB (2AVB), first‐degree AVB (1AVB), and no AVB (nAVB). The%VP was tabulated for each AVB status category.
Results:

Data were available from 322 patients of whom 129 received DDD(R) pacing with the MVP algorithm activated and 193 patients with DDD(R) pacing and the SAV+ function activated, each for a month period. MVP resulted in a significantly lower median%VP than SAV+ in all AVB categories except for p3AVB: nAVB (0.3 vs 2.9, P < 0.0001), 1AVB (0.9% vs 80.6%, P < 0.0001), 2AVB (37.6 vs 99.3, P< 0.002), e3AVB (1.2 vs 42.2, P = 0.02), p3AVB (98.9 vs 100, P = 1.00).
Conclusion:

MVP resulted in a greater reduction in%VP than SAV+ across all patient groups except persistent third‐degree AV block. The greatest reduction in%VP was observed in patients with mildly impaired AV conduction.
Variance of Peptidic Nerve Innervation in a Canine Model of Atrial Fibrillation Produced by Prolonged Atrial Pacing
Authors: QU XIUFEN , YU YANG , JIANG JIUYANG , BAI BING , GUO HONG , SONG YING 
Published: August 2010

Background:Long‐term rapid atrial pacing may result in nerve sprouting and sympathetic hyperinnervation in atrial fibrillation (AF) in dogs. Whether peptidic nerve is involved in neural remodeling is unclear.Method and Results:We performed rapid left atrial pacing in six dogs to induce sustained AF. Tissues from six healthy dogs were used as controls. Nerve was identified by immunocytochemical techniques. The degree of nerve innervation was quantified by measuring the amount of staining area for each antibody and the heterogeneity of nerve distribution was qualitatively studied. In dogs with AF, the density of growth‐associated protein 43 (GAP43) immunopositivenerve fibers in the left atrium (LA), atrial septum (AS), and right atrium (RA) was significantly (19,454.31 ± 1,592.81 μm2/mm2vs 1,673.41 ± 142.62 μm2/mm2P < 0.001, 3,931.26 ± 361.78 μm2/mm2vs 1,614.20 ± 140. 41 μm2/mm2P < 0.05 and 2,324.15 ± 1,123.77 μm2/mm2vs 1,620.47 ± 189.05 μm2/mm2P < 0.05, respectively) higher than the nerve density in control tissues. The density of (neuropeptide Y) NPY‐positive nerves in the, AS, and RA was (13,547.62 ± 2,983.37 μm2/mm2vs 703.72 ± 287.52 μm2/mm2P < 0.01, 2,689.22 ± 340.93 μm2/mm2vs 651.7 ± 283.02 μm2/mm2P < 0.01 and 1,574.70 ± 424.37 μm2/mm2vs 580.42 ± 188.12 μm2/mm2P < 0.001, respectively) higher than the nerve density in control tissues. At the same time, vasoactive intestinal polypeptide (VIP) positive nerve innervation shrank in dogs with AF. The density of VIP positive in LA, AS, and RA was statistically lower than the nerve density in control tissues, respectively. (110.48 ± 45.63μm2/mm2vs 1679.32 ± 1020.34μm2/mm2P < 0.01, 265.92 ± 52.51 μm2/mm2vs 2602.68 ± 1257.16μm2/mm2P < 0.001 and 609.56 ± 139.75μm2/mm2vs 2771.68 ± 779.08μm2/mm2P < 0.01, respectively)Conclusions:Combined with VIP‐ergic nerve denervation, significant nerve sprouting and NPY‐ergic nerve hyperinnervation are present in a canine model of sustained AF produced by prolonged atrial pacing.
Autonomic Response to Cardiac Dysfunction in Chronic Heart Failure: A Risk Predictor Based on Autonomic Information Flow
Authors: HOYER DIRK , MAESTRI ROBERTO , TERESA LA ROVERE MARIA , DOMENICO PINNA GIAN 
Published: August 2010

Background:

Chronic heart failure (CHF) is associated with a complex dysfunction of cardiac, cardiovascular, autonomic, and other mechanisms. Autonomic information flow (AIF) characteristics calculated from heart rate patterns were recently found as promising predictors of outcome in several cardiovascular diseases.
Aim:

To assess the prognostic value of AIF indices in CHF patients.
Methods:

We analyzed 24‐hour Holter recordings from 200 consecutive CHF patients in sinus rhythm and computed AIF over the shortest possible interval of an interbeat series, namely over one heart beat interval (BDnn), and over longer intervals (12.5–166.7 seconds, PDmVLF), which reflect slower heart rate modulations. End‐point for survival analysis over three years (Cox model) was total cardiac death. A prognostic model was built (backward elimination) considering known clinical and functional risk factors, and the ability of AIF indices to add prognostic information to this model assessed.
Results:

Out of candidate predictors, New York Heart Association class, left ventricular ejection fraction, peak VO2, and systolic pressure were selected as the variables with the highest joint predictive value. When entered into this model, both BDnn and PDmVLF added prognostic information (HR (95%CI): 1.76 (1.00–3.09), P = 0.05, 1.73 (1.05–2.85), P = 0.031 respectively). High risk was associated with reduced fast AIF and increased slower AIF.
Conclusion:

In CHF patients, AIF indices provide prognostic information independent of known risk factors.
Channelopathies in Children and Adults
Authors: WILDE ARTHUR A.M. 
Published: August 2010

In the last decade, pediatric cardiologists have witnessed a revolution in the knowledge of the pathophysiology of rare arrhythmias. The identification of the molecular basis of several hereditary arrhythmia syndromes has been instrumental in this development. Within 12 years the number of causal genes has increased from two in 1995 to at least 24 early 2007 (Table I). Based on this knowledge, established treatment strategies in the 1990s have been modified during the most recent years. This leads to timely and tailored treatment of (asymptomatic) gene carriers, both through personalized lifestyle advices and pharmacologically. At the same time and of equal importance, unaffected family members (noncarriers) can be reassured.

Number of Identified Genes Causal to Inherited Arrhythmia Syndromes in 1995 and Early 2007

1995
2007

Long QT syndrome(s)
2
10

Short QT syndrome
–
3

ST elevation right precordium, “RBBB,” SCD
–
4

Catecholamine‐induced PMVT/VF
–
3

Short‐coupled Torsades de Pointes
–
–

Isolated conduction disorders (AVN, BB)
–
1

Sinus node disease, atrial standstill
–
2
Rumen Ciliates of Musk‐Oxen (Ovibos moschatus Z.) from the Canadian Arctic1
Authors: Dehority Burk A. 
Published: August 2010

ABSTRACTSamples of rumen contents were obtained from 13 musk‐oxen living on Banks Island, N.W.T., Canada. Total protozoan numbers ranged from 38.5 to 124.6 times 104 per ml of rumen contents with a mean generic distribution of 52.4%Entodinium, 45.9%Diplodinium, and 1.7%Epidinium. A total of 18 protozoan species were found, six of which have not previously been observed in this host, i.e. D. (Diplodinium) costatum, D. (Ostracodinium) gracile, D. (Ostracodinium) trivesiculatum. D. (Eudiplodinium) medium, Epidinium quadricaudatum, and Epidinium parvicaudatum. Two new species of protozoa are described, Entodinium ovibos n. sp. and Diplodinium (Eudiplodinium) banksi n. sp.
PKX, the Causative Agent of Proliferative Kidney Disease (PKD) in Pacific Salmonid Fishes and Its Affinities with the Myxozoa1
Authors: Kent Michael L. , Hedrick Ronald P. 
Published: August 2010

ABSTRACTProliferative kidney disease (PKD), caused by an unclassified protozoan (PKX), is reported from Pacific salmon, Oncorhynchus tshawytscha (Walbaum) and O. kisutch (Walbaum), and steelhead trout, Salmo gairdneri Richardson, held at the Mad River Hatchery in California, USA. The cumulative mortality attributed to the disease was 95, 13, and 18% respectively. The mortalities were greatest at mean water temperatures of 12‐14°C during July 1983. The ultrastructure of the PKX organism and its associated pathology during clinical disease in all three species were consistent with those of the parasite in rainbow trout (Salmo gairdneri) as described in European outbreaks. Significant mortalities did not occur after August, at which time the parasite could no longer be detected in the salmon species. The steelhead continued to exhibit parasites in the kidney interstitium and epithelium and lumens of the tubules. Myxosporidan trophozoites and developing spores were also observed in the lumens of the kidney tubules of these fish. Although a mixed infection with another parasite may have occurred, evidence suggests that the myxosporidans are later stages of PKX. They were only observed in fish exposed to water with the infective stage and were particularly prominent in recovering fish. The PKX organism is similar to UBO, an unclassified protozoan of carp suspected to be an early stage of Sphaerospora renicola Dyková & Lom. Both parasites infect the blood and kidney, divide by endogeny, and are released by disintegration of the primary mother cell. The intraluminal myxosporean forms show similarities to Sphaerospora spp. in that they are monosporous and sporoblasts are formed within pseudoplasmodia. It is possible that PKX migrates to the lumen of the kidney tubule and subsequently sporulates. If the myxosporean forms are later stages of PKX, then it would belong to the phlyum Myxozoa.
Early Morphogenesis of Glugea‐lnduced Xenomas in Laboratory‐Reared Flounder
Authors: Weidner Earl 
Published: August 2010

ABSTRACTGlugea stephani‐infecled submucosal cells of laboratory‐reared winter flounder, Pseudopleuronectes americanus, change to unique giant cell xenomas. These cells hypertrophy while the intracellular Glugea propagate to high numbers in the cytoplasm and eventually overrun the host cell. The xenomas slowly reach 20‐25 muml;m (at 17°C) by day 10 after parasite invasion. These xenomas (eight often examined by electron microscopy) are coated with a mucus‐like envelope onto which is attached a layer of endothelial ceils. The 10‐day xenomas display (a) host cell endonuclear polyploidization and amitosis, (b) limited parasite growth and reproduction, and (c) a host cell cytoplasm structure similar to that seen in undifferentiated phagocytes. Glugea parasites do not induce obvious cell degenerative effects in 10‐day xenomas; the 20‐day xenomas are hypertrophied to 70‐100 m̈m. These cells are characterized by (a) a host cell component denuded of endoplasmic reticulum and phagosome membrane, (b) a reduction in host cell ribosomes and the disappearance of host cell cytoskeletal assemblages, including microtubules, and (c) a significant increase in vegetative Glugea within xenomas. Evidence indicates cytoplasmic calcium of the host cell xenoma is perturbed by the intracellular Glugea; the alterations in the host cell calcium domains may be a big factor in the induction of the block of mitosis in the host cell and in the disruption in its cytoskeletal controls.
Some Properties of Discharged Glugea hertwigi (Microsporida) Sporoplasms
Authors: Scarborough‐Bull Ann , Weidner Earl 
Published: August 2010

ABSTRACTGlugea hertwigi spores were activated to discharge sporoplasms in Medium 199 with 3% gelatin at pH 9.0; the liberated sporoplasms were transferred to a maintenance medium with 6% gelatin (pH 7.0) supplemented with 2 mM ATP and 10% (v/v) fetal calf scrum. The spherical sporoplasms (measuring 3.5‐4 m̈m in diameter) had single nuclei and had a cytoplasm rich in free ribosomes. Each G. hertwigi sporoplasm was initially bounded by an external (0.1‐0.2 m̈m) satellite body adjoining the plasma membrane. The satellites displayed ordered membrane and appeared to merge with the sporoplasm 15‐30 min after spore discharge. The external location of the satellite (in reference to the discharged sporoplasm) seems to be part of the normal sequence of events under the in vitro conditions provided. The surface of G. hertwigi sporoplasms does not bear an obvious surface coat; however, our cytochemical observations indicate the plasma membrane of the sporoplasm was somewhat responsive to concanavalin A‐peroxidase, colloidal iron, and native ferritin. During the short term incubations of sporoplasms with ferritin, the particles permeated membrane channels extending into the sporoplasm cytoplasm.
Trypanosoma cruzi: Histochemical Characterization of Parasitized Skeletal Muscle Fibers1
Authors: Teixeira M. Lucia , Dvorak James A. 
Published: August 2010

ABSTRACTC57B1/6 mice were infected with Brasil strain Trypanosoma cruzi trypomastigotes. The leg muscles of the mice were serial‐sectioned with a cryostat, and individual fibers were classified histochemically as type I or type II on the basis of succinic dehydrogenase or adenosine triphosphatase activity. Although markedly more type II fibers were present in the leg muscles, the percentage of infected type I fibers was nearly five‐fold higher than type II. This is the first demonstration of a preferential in vivo distribution of T. cruzi in muscle fibers based upon muscle type.
Lipid and Lipopolysaccharide‐Like Antigens of Leishmania Promastigotes1
Authors: Slutzky Gerald M. , Londner Mauricio V. , Greenblatt Charles L. 
Published: August 2010

ABSTRACTExtraction of whole promastigotes of Leishmania tropica major and L. donovani with a mixture of hexane and isopropanol (3:2) yielded three fractions containing immunological activity: 1) lipids, where the activity was determined by radioimmunoassay; 2) a lipopolysaccharide‐like (LPS‐like), water‐soluble precipitate, where activity was determined both by radioimmunoassay and double gel diffusion, and 3) the phenol: water extract of the lipid‐free promastigotes, where activity was followed by double gel diffusion.The use of a solid state, lipid‐based radioimmunoassay for detection of leishmanial antigens provided a sensitive measure of their activity with a considerable degree of species and serotype specificity. We found antibodies to leishmanial lipids in sera from immunized rabbits, convalescent mice, and human patients with confirmed cases of cutaneous leishmaniasis or kala azar. There was very little activity in normal human or animal sera. Analysis by SDS‐polyacrylamide gel electrophoresis of fractions from promastigotes surface‐labeled with galactose oxidase and sodium borotritiate and preliminary immunochemical characterization of the LPS‐like antigen showed that it contained galactose, but otherwise differed immunologically and chemically from excreted factor (EF), the best characterized leishmanial antigen.
Novobiocin‐Induced Ultrastructural Changes and Antagonism of DNA Synthesis in Trypanosoma cruzi Amastigotes Growing in Cell‐Free Medium
Authors: KERSCHMANN RUSSELL L. , WOLFSON JOHN S. , McHUGH GAIL L. , DICKERSIN G. RICHARD , HOOPER DAVID C. , SWARTZ MORTON N. 
Published: August 2010

ABSTRACTThe antimicrobial agent novobiocin, an inhibitor of the bacterial enzyme topoisomerase II (DNA gyrase), is known to antagonize Trypanosoma cruzi amastigotes growing in cell‐free medium. To determine sites of antagonism of novobiocin, the effects of drug on parasite ultrastructure and incorporation of radiolabeled precursors of DNA, RNA and protein into macromolecules were determined. The predominant ultrastructural abnormality seen after exposure to 0.40 mM novobiocin for 24 h was the presence of electron‐dense clumps in the mitochondrion‐kinetoplast organelle in 95 of 257 (37%) of cells, in comparison to no clumps seen in 110 drug‐free cells. In addition, in the nucleus, the karyosome was less distinct than in control cells and appeared to merge with the chromatin. In the radiolabcling studies, incorporation of thymidine was inhibited in a dose‐dependent fashion by novobiocin (0.16–0.80 mM) in a range of drug concentrations that also inhibited parasite growth. For 0.16 and 0.24 mM novobiocin, incorporation of thymidine was inhibited up to 65% relative to drug‐free control cells while uptake of uridine and leucine was unaltered. We interpret these ultrastructure and precursor‐incorporation studies as suggesting that (i) the mitochondrion‐kinetoplast and possibly the nucleus are sites of novobiocin antagonism of T. cruzi amastigotes and (ii) that novobiocin appears to antagonize DNA synthesis within these organisms. Whether the drug target is topoisomerase II, however, is as yet unknown.
5S Ribosomal RNA Sequence of Pneumocystis carinii and its Phylogenetic Association with “Rhizopoda/Myxomycota/Zygomycota Group”
Authors: WATANABFA JUN‐ICHI , HORI HIROSHI , TANABE KIYOKATSU , NAKAMURA YOSHIKAZU 
Published: August 2010

SUMMARYThe cytoplasmic 58 ribosomal RNA sequence from Pneumocystis carinii was determined and compared with those of 382 eukaryotes and an evolutionary tree was constructed to establish the phylogenetic position of Pneumocystis. The data suggest that Pneumocystis is associated with the RhizopodaAlyxomycota/ Zygomycota group but not with common fungi, such as Ascomycota or Basidiomycoia, nor with other protozoa.
Yeast Glucan in the Cyst Wall of Pneumocystis carinii
Authors: MATSUMOTO YOSHITSUGU , MATSUDA SHIN.II , TEGOSHI TATSUYA 
Published: August 2010

ABSTRACTUltrastructurally, the cyst wall of Pneumocystis carinii consists of an electron‐dense outer layer, an electron‐lucent middle layer, and an innermost plasmalemma. This is similar in appearance to the cell wall of some yeasts, e.g. Saccharomyces cerevisiae, which consists of an outer dense layer of mannan, a middle lucent layer of β−1,3‐glucan (yeast glucan) and an innermost plasmalemma. The cyst wall P. carinii, as well as the cell wall of S. cerevisiae, can be labeled by a variety of methods which stain polysaccharides, such as Gomori's methenamine silver (GMS) and by Aniline blue, a dye which selectively stains β‐1,3‐glucan. The treatment of P. carinii cysts with Zymolyase, which the key enzyme is β,3‐gIucan laminari‐pentaohydrolase, results in lysis of the outer 2 layers of the cyst wall and the loss of positive staining by both GMS and Aniline blue. The lysis of elements of the cyst wall of P. carinii is achieved under the same conditions and concentration at which Zymolyase lyses the outer 2 layers of the cell wall of viable cells of S. cerevisiae. These observations indicate that a major component of the cyst wall of P. carinii is β‐1,3‐glucan.
Some New Phenomena in Macronuclear Development of Euplotes patella Exconjugants
Authors: SATO KATSUYUKI 
Published: August 2010

ABSTRACTTwo new phenomena were observed during macronuclear development in E. patella. During the formation of giant chromosomes, the number of chromosomes decreased while individual chromosomes gradually became longer and thicker. Immediately before macronuclear elongation, ring‐like anlagen appeared, which did not contain chromatin at their centers. The course of macronuclear development in Euplotes is reconsidered in light of these findings.
Ultrastructural Observations on Life Cycle Stages of Pneumocystis carinii
Authors: RUFFOLO JOHN J. , CUSHION MELANIET. , WALZER PETER D. 
Published: August 2010

ABSTRACTAn ultrastructural study of life cycle stages of Pneumocystis carinii in infected rat lungs in situ was undertaken utilizing 8 different modes of fixation. Three of the fixatives employed gave good fixation of cysts and intracystic bodies, but for the trophic forms fixation was only fair. Both the trophic forms and intracystic bodies have nuclear pores. The mitochondria of the organism have cristac that appear lamellar. One of the fixation modes revealed a thin, electron‐dense layer on the outer surface of the cell wall, a “fuzzy coat” that had not been described previously. This material appears to mediate tight adhesion of trophic forms with other trophic forms, cysts, and with pneumocytcs of the lung alveolus.