bluuebunny/crossref_metadata_2025_split huggingface dataset:
Atrial fibrillation and minimally invasive coronary artery bypass grafting: Risk factor analysis
Authors: Mueller Xavier M. , Tevaearai Hendrik T. , Ruchat Patrick , Stumpe Frank , von Segesser Ludwig K. 
Published: October 2002

AbstractAtrial fibrillation (AF) is a frequent arrhythmia after conventional coronary artery bypass grafting. With the advent of minimally invasive technique for left internal mammary artery‐left anterior descending coronary artery (LIMA‐LAD) grafting, we analyzed the incidence and the risk factors of postoperative AF in this patient population. This prospective study involves all patients undergoing isolated LIMA‐LAD grafting with minimally invasive technique between January 1994 and June 2000. Twenty‐four possible risk factors for postoperative AF were entered into univariate and multivariate logistic regression analyses. Postoperative AF occurred in 21 of the 90 patients (23.3%) analyzed. Double‐ or triple‐vessel disease was present in 12/90 patients (13.3%). On univariate analysis, right coronary artery disease (p<0.01), age (p=0.01), and diabetes (p=0.04) were found to be risk factors for AF. On multivariate analysis, right coronary artery disease was identified as the sole significant risk factor (p=0.02). In this patient population, the incidence of AF after minimally invasive coronary artery bypass is in the range of that reported for conventional coronary artery bypass grafting. Right coronary artery disease was found to be an independent predictor, and this may be related to the fact that in this patient population the diseased right coronary artery was not revascularized at the time of the surgical procedure. For the same reason, this risk factor may find a broader application to noncardiac thoracic surgery.
Formation and use of covariation assessments in the real world
Authors: Coups Elliot J. , Chapman Gretchen B. 
Published: October 2002

AbstractIn this study we examined covariation assessments made using real‐world information held by individual participants about an important preventive health behaviour: receiving an influenza vaccine (‘flu shot’). Four hundred and seventy‐seven healthy adult participants completed a questionnaire, indicating both their personal experience and vicarious experience (knowledge of other people's experiences) with the flu shot and the flu. Additionally, participants provided a covariation assessment by indicating how effective they thought the flu shot is in preventing the flu. We examined whether the experience information was related to the covariation assessment, and whether it in turn was related to the decision to receive a flu shot. Our results indicated that people use a simple intuitive strategy to combine their personal experience information. For vicarious experience information, we found evidence for use of a normative strategy, as well as simpler intuitive strategies. Consistent with our hypothesis, both types of experience information were associated with the effectiveness judgement, which was subsequently related to the decision to obtain a flu shot. Practical applications of these findings are discussed. Copyright © 2002 John Wiley & Sons, Ltd.
Platelet spherocytosis: A new bleeding disorder
Authors: White James G. , de Alarcon Pedro A. 
Published: October 2002

AbstractThe present study evaluated a child with thrombocytopenia and a rare congenital bleeding disorder associated with platelet spherocytosis. Differential interference phase contrast microscopy (DIC) revealed that his platelets were spherical in form. Examination of thin sections in the electron microscope showed that his platelets were nearly devoid of microtubules (MT) and microtubule coils (MTC) that support the discoid shape in 100% of normal platelets. Immunofluorescence with a monoclonal antibody to tubulin, the precursor protein of MT, revealed bright rings in normal cells and diffuse fluorescence of patient platelets. The brightness of the fluorescence emitted by patient platelets was comparable to the diffuse fluorescence of normal platelets after chilling to dissolve intact MT, suggesting normal and patient cells contained comparable amounts of tubulin. Exposure of patient platelets to Taxol, an agent that stabilizes and induces MT, caused MT formation in 82% of patient platelets and MTC development in 11%, resulting in their conversion to discs. Glycoproteins GPIIb/IIIa and GPIb were present on patient platelets, and the cells contained normal numbers of dense bodies, ruling out storage pool disease. The patient's platelets adhered to and spread normally on glass but failed to undergo rapid, irreversible aggregation when stirred with agents that produced a complete response in normal discoid platelets, even when the patient's platelets were concentrated. The poor response of spherical platelets was associated with failure to become irregular and extend long filopodia. Thus, the spherical shape of patient platelets may contribute to the thrombocytopenia and to the clinical bleeding symptoms. Am. J. Hematol. 70:158–166, 2002. © 2002 Wiley‐Liss, Inc.
Cytogenetic findings in reactive lymphoid hyperplasia: Significance of non‐clonal t(3;14) and t(3;22)
Authors: Au Wing Y. , Horsman Douglas E. , Connors Joseph M. , Klasa Richard J. , Gascoyne Randy D. 
Published: October 2002

AbstractDespite several reports of the molecular detection of recurrent lymphoma translocations in reactive lymph nodes (LN), cytogenetic analysis is seldom performed on such cases. We report the clinical and cytogenetic analysis results on 30 reactive LN. Of these, 17 cases yielded either no growth (n = 9) or normal metaphases only (n = 8), and seven of the 17 patients subsequently developed lymphoma. Lymphoma developed in all 10 patients with a clonal karyotype (median of 2.6 months). Three patients (1 HIV‐positive) had non‐clonal t(3;14) or t(3;22). Their lymphadenopathy resolved spontaneously, and none progressed to lymphoma at 4–6 years of follow‐up. Molecular methods detected a small B‐cell clone in one case and an oligoclonal B‐cell population in the other. Cytogenetic analysis may be useful for interpreting cases of lymphoid hyperplasia. A clonal abnormality is highly predictive of concurrent and/or subsequent lymphoma. A lymphoma‐specific but non‐clonal abnormality does not necessarily herald the development of subsequent lymphoma. Am. J. Hematol. 70:133–138, 2002.© 2002 Wiley‐Liss, Inc.
Spectrum of β‐thalassemia mutations and their association with allelic sequence polymorphisms at the β‐globin gene cluster in an eastern Indian population
Authors: Kukreti Ritushree , Dash Debasis , K E Vineetha , Chakravarty Sanchita , Kr Das Swapan , De Madhusnata , Talukder Geeta 
Published: October 2002

AbstractIn this report, the spectrum of β‐thalassemia mutations and genotype‐to‐phenotype correlations were defined in large number of patients (β‐thalassemia carriers and major) with varying disease severity in an Eastern Indian population mainly from the state of West Bengal. The five most common β‐thalassemia mutations were detected, which included IVS1‐5 (G→C), codon 15 (G→A), codon 26 (G→A), codon 30 (G→C), and codon 41/42 (−TCTT). These accounted for 85% in 80 β‐thalassemic alleles deciphered from 56 patients, including β‐thalassemia major and carriers, and 15% of alleles remained uncharacterized in these patients. Expression of the human β‐globin gene is regulated by an array of cis‐acting DNA elements, including five DNase I hypersensitive sites (HSs) in the locus control region (LCR), promoters that incorporate certain silencer elements, and enhancers at 3′ of the β‐globin gene. For detailed studies and to understand the molecular basis of β‐thalassemia, we studied two groups of subjects: a group of 12 patients from four families having β‐thalassemia major and carrier phenotype and a control group of 26 healthy individuals. In these two groups, we examined portions of the β‐globin gene locus control region HSs 1, 2, 3, and 4, which included the (CA)x(TA)y repeat motif, the (AT)xNy(AT)z repeat motif, the inverted repeat sequence TGGGGACCCCA, the promoter region of the Gγ‐globin gene, an (AT)x(T)y repeat 5′ of the silencer region, and the β‐globin gene and its 3′ flanking region. We investigated the allelic sequence polymorphisms in these regions and their association with the β‐thalassemia mutations to know the possible genotype–phenotype relationship in β‐thalassemia patients. An analysis of cis‐acting regulatory regions showed varied sequence haplotypes associated with some frequent β‐thalassemia mutations in this Eastern Indian population. Am. J. Hematol. 70:269–277, 2002. © 2002 Wiley‐Liss, Inc.
Arsenic trioxide in the treatment of newly diagnosed acute promyelocytic leukemia: A single center experience
Authors: Mathews Vikram , Balasubramanian Poonkuzhali , Shaji Ramachandran Velayudhan , George Biju , Chandy Mammen , Srivastava Alok 
Published: October 2002

AbstractArsenic trioxide (As2O3) has been found effective in the treatment in the treatment of acute promyelocytic leukemia (APML). Most studies with As2O3 involve patients with APML who have relapsed following standard therapy. Between January 1998 and July 2000, 14 patients were recruited for an ongoing trial of As2O3 in the treatment of newly diagnosed APML. Arsenic trioxide was administered at a dose of 10 mg/day until complete remission (CR) was achieved. Afterward, a consolidation course and a maintenance schedule consisting of As2O3 as a single agent were administered over 6 months. There were 3 early deaths related to intra‐cerebral hemorrhage: two on day 3 and one on day 4. Of the 11 evaluable patients, one died on day 21 secondary to uncontrolled sepsis, while the remaining 10 (91%) have attained CR. The average time to CR was 52.3 days (range: 34–70 days). One patient developed an isolated central nervous system (CNS) relapse and subsequently went into a second CR following therapy with triple intrathecal chemotherapy, cranial irradiation, and an additional 4‐week course of systemic As2O3. This patient, as well as the remaining nine, has continued to remain in CR at a median follow up of 15 months (range: 2−33 months). Eight out of 10 patients achieved molecular remission at variable periods during their consolidation and maintenance schedules. One patient developed an ATRA syndrome and was administered daunorubicin (40 mg/day) for 2 days. The side effects with this therapy were minimal and did not require cessation of therapy in any patient. There was no significant hepatic toxicity. In our experience, arsenic trioxide is effective in inducing and maintaining remission in patients with APML with minimal side effects. The optimal regimen and total dose required need to be defined. Am. J. Hematol. 70:292–299, 2002. © 2002 Wiley‐Liss, Inc.
Age‐related decrease in energy expenditure at rest parallels reductions in mass of internal organs
Authors: Puggaard Lis , Bjørnsbo Kirsten Schroll , Kock Kirsten , Lüders Kurt , Thobo‐Carlsen Brit , Lammert Ole 
Published: October 2002

AbstractThis study explores to what extent the mass of internal organs may impact the age‐related decrease in energy expenditure at rest (EErest). The relationship between direct measurements of EErest in elderly women and predicted EErest based on equations deriving from the metabolic activity in tissue from younger women were also elucidated. Body composition of elderly women was measured by an impedance method. EErest was measured by the Douglas bag method after an overnight fast. These data were compared with predicted values of EErest based on equations derived from studies in younger women. The mass of internal organs was obtained from autopsy material. Young women (mean age 31.7 years, range 14–60, n = 104) and elderly women of 65 years (n = 22), 75 years (n = 26), and 85 years (n = 31) participated in this study. Autopsy data were obtained from women (n = 238) from the same birth cohorts as the elderly women who died at ages 42–87 years. EErest showed a progressive age‐related decline, which appeared to parallel a similar reduction in the mass of internal organs derived from autopsy material of women who died at the same ages. In contrast, FFM was identical in the group of 65 and 75‐year‐old women, but was lower in the 85‐year‐old women. Predicted and measured EErest revealed a strong correlation in elderly women. Modest reductions in the mass of internal organs with a high metabolic rate appear to contribute markedly to the decline in EErest observed in aging. Further, it is also possible to predict EErest from the body composition of elderly women using equations developed from younger women. Am. J. Hum. Biol. 14: 486–493, 2002. © 2002 Wiley‐Liss, Inc.
Anything but beryllium: The beryllium industry's corruption of safety information
Authors: Egilman David , Bagley Sarah , Connolly Shannon 
Published: October 2002

AbstractTo the Editor:Beryllium manufacturers have long recognized the relationship between marketing, compensation claims and fear of Be toxicity. In response, they sponsored researchers who manipulated and influenced medical literature to minimize the consequences of Be exposure to workers and members of the community. This dates back to the 1940s, when the Atomic Energy Council(AEC)Advisory Board on Medicine and Biology established the following policy: "If specific locations or activities of the Atomic Energy Commission and/or its contractors are closely associated with statements and information which would invite or tend to encourage claims against the Atomic Energy Commission or its contractors, such portions of articles to be published should be reworded or deleted" [AEC memo, 1947].
No evidence for linkage of liability to autism toHOXA1in a sample from the CPEA network
Authors: Devlin Bernie , Bennett Pamela , Cook, Edwin H. , Dawson Geraldine , Gonen David , Grigorenko Elena L. , McMahon William , Pauls David , Smith Moyra , Spence M. Anne ,   CPEA Genetics Network, Schellenberg Gerard D. 
Published: October 2002

AbstractA recent study by Ingram et al. [2000b: Teratology 62:393–405] suggests aHis73Argpolymorphism (A:G) inHOXA1contributes substantially to a liability for autism. Using 68 individuals diagnosed with Autism Spectrum Disorders, they found a significant dearth of G homozygotes and biased transmission of G alleles from parents to affected offspring, especially from mothers. Because the connection betweenHOXA1and liability to autism is compelling, we attempted to replicate their finding using a larger, independent sample from the Collaborative Programs of Excellence in Autism (CPEA) network. In our data, genotype frequencies conform to Hardy‐Weinberg equilibrium; allele transmissions meet Mendelian expectations; and there is no obvious sex‐biased allele transmission. Based on our sample size, calculations suggest that we would have at least 95% power to detect linkage and association even if the A:G polymorphism were to account for only 1% of the heritability of autism. Therefore, although we cannot exclude the possibility that the samples in the two studies are intrinsically different, our data from our sample argue against a major role for HOXA1His73Argin liability to autism. © 2002 Wiley‐Liss, Inc.
Mouse models for mitochondrial disease
Authors: Wallace Douglas C. 
Published: October 2002

AbstractMutations in mitochondrial genes encoded by both mitochondrial DNA (mtDNA) and nuclear DNA (nDNA) genes have been implicated in a wide range of neuromuscular diseases. MtDNA base substitution and rearrangement mutations generally inactivate one or more tRNA or rRNA genes and can cause myopathy, cardiomyopathy, cataracts, growth retardation, diabetes, etc. nDNA mutations can cause Leigh syndrome, cardiomyopathy, and nephropathy, due to defects in oxidative phosphorylation (OXPHOS) enzyme complexes; cartilage‐hair hypoplasia (CHH) and mtDNA depletion syndrome, through defects in mitochondrial nucleic acid metabolism; and ophthalmoplegia with multiple mtDNA deletions, caused by adenine nucleotide translocator‐1 (ANT1) mutations. Mouse models have been prepared that recapitulate a number of these diseases. The mtDNA 16S rRNA chloramphenicol (CAP) resistance mutation was introduced into the mouse female germline and caused cataracts and rod and cone abnormalities in chimeras and neonatal lethal myopathy and cardiomyopathy in mutant animals. A mtDNA deletion was introduced into the mouse germline and caused myopathy, cardiomyopathy, and nephropathy. Conditional inactivation of the nDNA mitochondrial transcription factor (Tfam) gene in the heart resulted in neonatal lethal cardiomyopathy, while its inactivation in the pancreatic β‐cells caused diabetes. The ATP/ADP ratio was implicated in mitochondrial diabetes through transgenic modification of the β‐cell ATP‐sensitive K+ channel (KATP). Mutational inactivation of the mouse Ant1 gene resulted in myopathy, cardiomyopathy, and multiple mtDNA deletions in association with elevated reactive oxygen species (ROS) production. Inactivation of uncoupler proteins (Ucp) 1–3 revealed that mitochondrial Δψ regulated ROS production. The role of mitochondrial ROS toxicity in disease and aging was confirmed by inactivating glutathione peroxidase (GPx1), resulting in growth retardation, and by total and partial inactivation of Mn superoxide dismutase (MnSOD; Sod2), resulting in neonatal lethal dilated cardiomyopathy and accelerated apoptosis in aging, respectively. The importance of mitochondrial ROS in degenerative diseases and aging was confirmed by treating Sod2 −/− mice and C. elegans with catalytic antioxidant drugs. © 2001 Wiley‐Liss, Inc.
Mitochondria and degenerative disorders
Authors: Orth M. , Schapira A.H.V. 
Published: October 2002

AbstractIn mammalian cells, mitochondria provide energy from aerobic metabolism. They play an important regulatory role in apoptosis, produce and detoxify free radicals, and serve as a cellular calcium buffer. Neurodegenerative disorders involving mitochondria can be divided into those caused by oxidative phosphorylation (OXPHOS) abnormalities either due to mitochondrial DNA (mtDNA) abnormalities, e.g., chronic external ophthalmoplegia, or due to nuclear mutations of OXPHOS proteins, e.g., complex I and II associated with Leigh syndrome. There are diseases caused by nuclear genes encoding non‐OXPHOS mitochondrial proteins, such as frataxin in Friedreich ataxia (which is likely to play an important role in mitochondrial‐cytosolic iron cycling), paraplegin (possibly a mitochondrial ATP‐dependent zinc metalloprotease of the AAA‐ATPases in hereditary spastic paraparesis), and possibly Wilson disease protein (an abnormal copper transporting ATP‐dependent P‐type ATPase associated with Wilson disease). Huntingon disease is an example of diseases with OXPHOS defects associated with mutations of nuclear genes encoding non‐mitochondrial proteins such as huntingtin. There are also disorders with evidence of mitochondrial involvement that cannot as yet be assigned. These include Parkinson disease (where a complex I defect is described and free radicals are generated from dopamine metabolism), amyotrophic lateral sclerosis, and Alzheimer disease, where there is evidence to suggest mitochondrial involvement perhaps secondary to other abnormalities. © 2001 Wiley‐Liss, Inc.
Distribution, population structure, and conservation of lion‐tailed macaques (Macaca silenus) in the Anaimalai Hills, Western Ghats, India
Authors: Singh Mewa , Singh Mridula , Kumar M. Ananda , Kumara H.N. , Sharma A.K. , Kaumanns W. 
Published: October 2002

AbstractThe lion‐tailed macaque is an endangered species, and hence it is necessary that the remaining populations in the rainforests of the Western Ghats, India, be located and their habitats assessed for effective conservation. The Anaimalai Hills in the state of Tamil Nadu harbor 31 groups of lion‐tailed macaques. However, the rainforest in these hills is highly fragmented. Since lion‐tailed macaques are typically arboreal, the groups have become isolated. Two large rain‐forest complexes in these hills harbor 12 and seven groups, respectively, and the remaining 12 groups inhabit small, isolated forest fragments. Group size ranges from six to 53 individuals, with a mean size of 16.3. In the small forest fragments, the standard deviation (SD) of group size was considerably higher than it was in the larger forest complexes. The disturbed fragments also had a higher variability in group size than the relatively undisturbed habitats. It is believed that fragmentation may impede male migration. We suggest that the fragments be managed in such a way that male migration among groups can be facilitated to overcome the potential effects of isolation. © 2002 Wiley‐Liss, Inc.
Clinical variability in 3‐hydroxy‐2‐methylbutyryl‐coa dehydrogenase deficiency
Authors: Ensenauer Regina , Niederhoff Helmut , Ruiter Jos P. N. , Wanders Ronald J. A. , Schwab K. Otfried , Brandis Matthias , Lehnert Willy 
Published: October 2002

AbstractWe report the identification of two new 7‐year‐old patients with 3‐hydroxy‐2‐methylbutyryl‐CoA dehydrogenase deficiency, a recently described inborn error of isoleucine metabolism. The defect is localized one step above 3‐ketothiolase, resulting in a urinary metabolite pattern similar to that seen for deficiency of the latter. One patient has progressive neurodegenerative symptoms, whereas the clinical phenotype of the other patient is characterized by psychomotor retardation without loss of developmental milestones. A short‐term biochemical response to an isoleucine‐restricted diet was observed in both children.
In vivo study indicating loss of intracortical inhibition in tumor‐associated epilepsy
Authors: Irlbacher Kerstin , Brandt Stephan A. , Meyer Bernd‐Ulrich 
Published: October 2002

AbstractTranscranial magnetic stimulation was performed in 2 patients with focal motor seizures in the right hand caused by a circumscribed tumor process affecting the left precentral gyrus. In both cases, paired‐pulse transcranial magnetic stimulation showed a loss of intracortical inhibition for interstimulus intervals of 2 to 4msec that was replaced by an enormous facilitation in the lesioned hand motor cortex. The uniform impairment of inhibitory mechanisms in epileptogenic tumors with different histologies suggests a common, nonspecific cause of tumor‐related epileptogenesis.
Sudomotor testing predicts the presence of neutralizing botulinum A toxin antibodies
Authors: Birklein Frank , Walther Dirk , Bigalke Hans , Winterholler Martin , Erbguth Frank 
Published: October 2002

AbstractThe increasing number of patients being treated with botulinum toxin A complex (BoNT/A) has led to a higher incidence of neutralizing anti‐BoNT/A antibodies (ABAs). Because BoNT/A is known to inhibit sweating, here we report sudometry as a possibility for predicting the presence of ABA. Sixteen patients suffering from spasmodic torticollis were selected: in 2 patients, BoNT/A treatment continued to be effective, in 9 patients, the treatment effect was impaired, and in 5 patients, secondary treatment failure developed. BoNT/A (100 mouse units, Dysport; Ipsen Pharma, Berkshire, United Kingdom) was injected subcutaneously into the lateral calves. Sweating was visualized with iodine starch staining. In addition, quantitative sudomotor axon reflex testing was performed at the injection site. Individual ABA titers were determined with a mouse bioassay. Results of sudometry significantly correlated with the BoNT/A treatment success. The quantitative sudomotor axon reflex testing was 0.58 ± 0.63 fraction of the normal mean in patients with treatment failure, 0.18 ± 0.13 fraction of the normal mean in those who responded partially, and 0 in responders (p < 0.01). Accordingly, the areas of the anhidrotic skin after subcutaneous injections were 4.5 ± 10.3cm2, 32.7 ± 16.5cm2, and 62cm2 (p < 0.01). Discrimination analysis indicated that the presence of ABA (6 ABA‐positive and 10 ABA‐negative) could be predicted correctly in all patients from the results of sudometry. Therefore, sudometry is a useful tool for identifying patients with neutralizing ABAs and might be helpful for identifying reasons for BoNT/A treatment failure.