bluuebunny/crossref_metadata_2025_split huggingface dataset:
Clinical relevance of short‐term day‐time breathing disorders in chronic heart failure patients
Authors: La Rovere Maria Teresa , Pinna Gian Domenico , Maestri Roberto , Robbi Elena , Mortara Andrea , Fanfulla Francesco , Febo Oreste , Sleight Peter 
Published: July 2007

AbstractBackground:Periodic Breathing (PB, waxing and waning of tidal volume in which hyperventilation alternates with periods of apnoea or hypopnoea), is common during sleep and wakefulness in patients with Heart Failure (HF) and may increase mortality.Aim:To assess the effect of short‐term, day‐time PB on prognosis, in HF patients.Methods:We prospectively studied 380 consecutive HF referrals who had a 10 min, supine day‐time respiratory recording. We related PB (adjusted for known predictors) to total cardiac mortality, during a median follow‐up of 41 months.Results:Day‐time PB occurred in 145/380 patients who had more severe HF and more compromised left ventricular function (p<0.005). Survival curves began to separate after 10 months and diverged steadily over the next 4 years with a cumulative risk of 41% (PB) vs 26% (No‐PB), p<0.002. PB was independently predictive of increased cardiac mortality when entered into a clinical prognostic model (including NYHA Class, LVEF, LVEDD, Systolic Arterial Pressure, beta‐blocker treatment, peak VO2 and blood urea) with a RR: 1.8, 95% CI 1.20–2.81.Conclusion:In advanced HF the presence of PB during a short day‐time recording adds to known predictors of cardiac mortality. This may have practical implications for trials of HF therapy.
Parametric instabilities of circularly polarized small-amplitude Alfvén waves in Hall plasmas
Authors: RUDERMAN MICHAEL S. , CAILLOL PHILIPPE 
Published: July 2007

AbstractWe study the stability of circularly polarized Alfvén waves (pump waves) in Hall plasmas. First we re-derive the dispersion equation governing the pump wave stability without making anad hocassumption about the dependences of perturbations on time and the spatial variable. Then we study the stability of pump waves with small non-dimensional amplitudea(a≪ 1) analytically, restricting our analysis tob< 1, wherebis the ratio of the sound and Alfvén speed. Our main results are the following. The stability properties of right-hand polarized waves are qualitatively the same as in ideal MHD. For any values ofband the dispersion parameter τ they are subject to decay instability that occurs for wave numbers from a band with width of ordera. The instability increment is also of ordera. The left-hand polarized waves can be subject, in general, to three different types of instabilities. The first type is the modulational instability. It only occurs whenbis smaller than a limiting value that depends on τ. Only perturbations with wave numbers smaller than a limiting value of orderaare unstable. The instability increment is proportional toa2. The second type is the decay instability. It has the same properties as in the case of right-hand polarized waves; however, it occurs only whenb< 1 τ. The third type is the beat instability. It occurs for any values ofband τ, and only perturbations with the wave numbers from a narrow band with the width of ordera2are unstable. The increment of this instability is proportional toa2, except for τ close to τcwhen it is proportional toa, where τcis a function ofb.
Respiratory infection in congenital cardiac disease. Hospitalizations in young children in Spain during 2004 and 2005: the CIVIC Epidemiologic Study
Authors: Medrano Constancio , Garcia-Guereta Luis , Grueso Josefina , Insa Beatriz , Ballesteros Fernando , Casaldaliga Jaume , Cuenca Victorio , Escudero Fuensanta , Garcia de la Calzada Lola , Luis Maite , Luque Manuel , Mendoza Alberto , Prada Fredy , del Mar Rodríguez Maria , Suarez Pedro , Quero Concepción , Guilera Magda 
Published: July 2007

AbstractObjectivesTo evaluate the rate of hospitalization for acute respiratory tract infection in children less than 24 months with haemodynamically significant congenital cardiac disease, and to describe associated risk factors, preventive measures, aetiology, and clinical course.Materials and methodsWe followed 760 subjects from October 2004 through April 2005 in an epidemiological, multicentric, observational, follow-up, prospective study involving 53 Spanish hospitals.ResultsOf our cohort, 79 patients (10.4%, 95% CI: 8.2%–12.6%) required a total of 105 admissions to hospital related to respiratory infections. The incidence rate was 21.4 new admissions per 1000 patients-months. Significant associated risk factors for hospitalization included, with odds ratios and 95% confidence intervals shown in parentheses: 22q11 deletion (8.2, 2.5–26.3), weight below the 10th centile (5.2, 1.6–17.4), previous respiratory disease (4.5, 2.3–8.6), incomplete immunoprophylaxis against respiratory syncytial virus (2.2, 1.2–3.9), trisomy 21 (2.1, 1.1–4.2), cardiopulmonary bypass (2.0, 1.1–3.4), and siblings aged less than 11 years old (1.7, 1.1–2.9). Bronchiolitis (51.4%), upper respiratory tract infections (25.7%), and pneumonia (20%) were the main diagnoses. An infectious agent was found in 37 cases (35.2%): respiratory syncytial virus in 25,Streptococcus pneumoniaein 5, and Haemophilus influenzae in 4. The odds ratio for hospitalization due to infection by the respiratory syncytial virus increases by 3.05 (95% CI: 2.14 to 4.35) in patients with incomplete prophylaxis. The median length of hospitalization was 7 days. In 18 patients (17.1%), the clinical course of respiratory infection was complicated and 2 died.ConclusionsHospital admissions for respiratory infection in young children with haemodynamically significant congenital cardiac disease are mainly associated with non-cardiac conditions, which may be genetic, malnutrition, or respiratory, and to cardiopulmonary bypass. Respiratory syncytial virus was the most commonly identified infectious agent. Incomplete immunoprophylaxis against the virus increased the risk of hospitalization.
Common themes and variations in the rhodanese superfamily
Authors: Cipollone Rita , Ascenzi Paolo , Visca Paolo 
Published: July 2007

AbstractThe rhodanese homology domain is a ubiquitous fold found in several phylogenetically related proteins encoded by eubacterial, archeal, and eukaryotic genomes. Although rhodanese‐like proteins share evolutionary relationships, analysis of their sequences highlights that they are so heterogeneous to form the rhodanese superfamily. The variability occurs at different levels including sequence, active site loop length, presence of a critical catalytic Cys residue, and domain arrangement. Even within the same genome, multiple genes encode rhodanese‐like proteins presenting with variably arranged rhodanese domain(s): as single or tandem domain(s), or combined with other protein domain(s). Given the highly variable organization of the rhodanese domain(s) and the context where it is found, here we review the structural organization and function of the rhodanese‐like proteins. The overview of the most recent findings about rhodanese allow us to depict a superfamily of versatile proteins relying on persulfide chemistry to accomplish cellular functions spanning from resistance to environmental threats, such as cyanide, and key cellular reactions related to sulfur metabolism and progression of cell cycle.
IUBMB Life, 59: 51‐59, 2007
Calcium, iron and neuronal function
Authors: Hidalgo Cecilia , Núñez Marco T. 
Published: July 2007

AbstractCalcium and iron play dual roles in neuronal function: they are both essential but when present in excess they cause neuronal damage and may even induce neuronal death. Calcium signals are required for synaptic plasticity, a neuronal process that entails gene expression and which is presumably the cellular counterpart of cognitive brain functions such as learning and memory. Neuronal activity generates cytoplasmic and nuclear calcium signals that in turn stimulate pathways that promote the transcription of genes known to participate in synaptic plasticity. In addition, evidence discussed in this article shows that iron deficiency causes learning and memory impairments that persist following iron repletion, indicating that iron is necessary for normal development of cognitive functions. Recent results from our group indicate that iron is required for long‐term potentiation in hippocampal CA1 neurons and that iron stimulates ryanodine receptor‐mediated calcium release through ROS produced via the Fenton reaction leading to stimulation of the ERK signaling pathway. These combined results support a coordinated action between iron and calcium in synaptic plasticity and raise the possibility that elevated iron levels may contribute to neuronal degeneration through excessive intracellular calcium increase caused by iron‐induced oxidative stress.
IUBMB Life, 59: 280‐285, 2007
The tammar wallaby: A model to examine endocrine and local control of lactation
Authors: Brennan Amelia J. , Sharp Julie A. , Digby Matthew R. , Nicholas Kevin R. 
Published: July 2007

AbstractWORTH A SECOND LOOK
From time to time we republish review articles from the Australian Biochemist, the magazine of the Australian Society for Biochemistry and Molecular Biology Inc. This exposes these excellent reviews to a much wider and different readership. Here we republish a review on the tammar wallaby that originally appeared in the Australian Biochemist, volume 57, no. 2, August 2006.
We are most grateful for the permission of the authors and of Rebecca Lew, the Editor of the Australian Biochemist, to republish the review. Dr Lew is also an IUBMB Life Editor.
Marsupials, such as the tammar wallaby (Macropus eugenii), have adopted a reproductive strategy that is very different to eutherians. Both the rate of production and the composition of milk changes progressively during the lactation cycle to meet the nutritional demands of an altricial young. The tammar therefore provides a valuable model to study changes in milk composition, and in particular the genes that code for proteins secreted in the milk, to more accurately assess the role of gene products regulating either development of the young or mammary function.
IUBMB Life, 59: 146‐150, 2007
Gene response elements, genetic polymorphisms and epigenetics influence the human dietary requirement for choline
Authors: Zeisel Steven H. 
Published: July 2007

AbstractRecent progress in the understanding of the human dietary requirement for choline highlights the importance of genetic variation and epigenetics in human nutrient requirements. Choline is a major dietary source of methyl‐groups (one of choline's metabolites, betaine, participates in the methylation of homocysteine to form methionine); also choline is needed for the biosynthesis of cell membranes, bioactive phospholipids and the neurotransmitter acetylcholine. A recommended dietary intake for choline in humans was set in 1998, and a portion of the choline requirement can be met via endogenous de novo synthesis of phosphatidylcholine catalyzed by phosphatidylethanolamine N‐methyltransferase (PEMT) in the liver. Though many foods contain choline, many humans do not get enough in their diets. When deprived of dietary choline, most adult men and postmenopausal women developed signs of organ dysfunction (fatty liver, liver or muscle cell damage, and reduces the capacity to handle a methionine load, resulting in elevated homocysteine). However, only a portion of premenopausal women developed such problems. The difference in requirement occurs because estrogen induces expression of the PEMT gene and allows premenopausal women to make more of their needed choline endogenously. In addition, there is significant variation in the dietary requirement for choline that can be explained by common polymorphisms in genes of choline and folate metabolism. Choline is critical during fetal development, when it alters DNA methylation and thereby influences neural precursor cell proliferation and apoptosis. This results in long term alterations in brain structure and function, specifically memory function.
IUBMB Life, 59: 380 ‐ 387, 2007
Heme binding to albuminoid proteins is the result of recent evolution
Authors: Fasano Mauro , Fanali Gabriella , Leboffe Loris , Ascenzi Paolo 
Published: July 2007

AbstractWe hypothesize that the structure of the heme binding site of paralogous albuminoids alpha‐fetoprotein and serum albumin has evolved from the ancestor vitamin D binding protein through the 'phylogenetic intermediate' afamin, the most recently discovered albuminoid. Heme binding to plasma proteins should serve not only as a buffer for heme homeostasis, avoiding heme binding to lipoproteins with the consequent oxidative stress, but also for heme transfer to the liver, complementing the function of hemopexin.
iubmb Life, 59: 436‐440, 2007
INK4 proteins, a family of mammalian CDK inhibitors with novel biological functions
Authors: Cánepa Eduardo T. , Scassa María E. , Ceruti Julieta M. , Marazita Mariela C. , Carcagno Abel L. , Sirkin Pablo F. , Ogara María F. 
Published: July 2007

AbstractThe cyclin D‐Cdk4‐6/INK4/Rb/E2F pathway plays a key role in controlling cell growth by integrating multiple mitogenic and antimitogenic stimuli. The members of INK4 family, comprising p16INK4a, p15INK4b, p18INK4c, and p19INK4d, block the progression of the cell cycle by binding to either Cdk4 or Cdk6 and inhibiting the action of cyclin D. These INK4 proteins share a similar structure dominated by several ankyrin repeats. Although they appear to be structurally redundant and equally potent as inhibitors, the INK4 family members are differentially expressed during mouse development. The striking diversity in the pattern of expression of INK4 genes suggested that this family of cell cycle inhibitors might have cell lineage‐specific or tissue‐specific functions. The INK4 proteins are commonly lost or inactivated by mutations in diverse types of cancer, and they represent established or candidate tumor suppressors. Apart from their capacity to arrest cells in the G1‐phase of the cell cycle they have been shown to participate in an increasing number of cellular processes. Given their emerging roles in fundamental physiological as well as pathological processes, it is interesting to explore the diverse roles for the individual INK4 family members in different functions other than cell cycle regulation. Extensive studies, over the past few years, uncover the involvement of INK4 proteins in senescence, apoptosis, DNA repair, and multistep oncogenesis. We will focus the discussion here on these unexpected issues.
iubmb Life, 59: 419‐426, 2007
Let's stick together: The role of the Fras1 and Frem proteins in epidermal adhesion
Authors: Short Kieran , Wiradjaja Fenny , Smyth Ian 
Published: July 2007

AbstractThe Fras1 and Frem extracellular matrix proteins play critical roles in epithelial‐mesenchymal interaction during embryonic development. Loss of function in humans results in a recessive embryonic blistering disorder called Fraser syndrome. Inactivation of these proteins, or the proteins with which they interact (e.g., Grip1) has also been shown to underlie members of the 'bleb' family of classic mouse mutants which provide a valuable model of Fraser syndrome. Recent studies supporting direct interactions between the Fras1 and Frem proteins, combined with more rigorous elucidation of their developmental regulation, have shed new light on their activity. We summarize the findings to date, bringing new insight into their role in the regulation of epidermal‐basement membrane adhesion and organogenesis during development.
iubmb Life, 59: 427‐435, 2007
Blocking SCF/c‐Kit signal did not inhibit the proliferation of cultured liver progenitor cells
Authors: Jin Caixia , Li Wenlin , Xu Fang , Zhu Ji , He Zhiying , Hu Yiping 
Published: July 2007

AbstractOval cells are the putative liver stem cells that proliferate during hepatocarcinogenesis and chemically‐induced severe liver injury. Antigens traditionally associated with haematopoietic cells, such as c‐Kit, have been reported to be expressed by oval cells. Previous studies suggested that stem cell factor (SCF) and c‐Kit were critical to oval cell development. However, the role of SCF/c‐Kit signals in oval cell proliferation still remains unclear. Recently, we reported the establishment of oval cell‐derived liver epithelial progenitor cells (LEPCs). In this work, we showed LEPCs co‐expressed c‐Kit and its ligand SCF. The involvement of SCF/c‐Kit signals in LEPCs proliferation was investigated either by exposing LEPCs to c‐Kit inhibitors (STI571 and AG1296), SCF, anti‐SCF neutralized antibody or by using small interfering RNA to knock‐down c‐Kit expression. Our data demonstrate that blocking SCF/c‐Kit signal did not inhibit the proliferation of LEPCs, which suggest SCF/c‐Kit is not necessary for the proliferation of oval cells, at least for the cultured oval cell counterpart LEPCs.
iubmb Life, 59: 458‐464, 2007
Time‐dependent inhibition of human drug metabolizing cytochromes P450 by tricyclic antidepressants
Authors: Polasek Thomas M. , Miners John O. 
Published: July 2007

WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT• Much of the literature evidence for mechanism‐based inactivation (MBI) of CYP by tricyclic antidepressants is limited to studies in rat liver microsomes.• One report from this laboratory characterized MBI of human recombinant CYP2C8 by nortriptyline.WHAT THIS STUDY ADDS• Tricyclic antidepressants form alkylamine metabolite‐intermediate complexes with human recombinant CYP enzymes (expressed inEscherichia coli) relatively easily, resulting in time‐dependent inhibition.• Evidence to support similar irreversible inhibition using human liver microsomal (HLM) fractions is limited.• HLM and recombinant CYP (expressed inE. coli) are not equivalent enzyme sources for evaluating the time‐dependent inhibition of human drug metabolizing CYP that is associated with some drugs.AIMSTo investigate time‐dependent inhibition (TDI) of human drug metabolizing CYP enzymes by tricyclic antidepressants (TCAs).METHODSCYP1A2, CYP2C9, CYP2C19, CYP2D6 and CYP3A/CYP3A4 activities were investigated following co‐ and preincubation with TCAs using human liver microsomes (HLM) and human recombinant CYP proteins (expressed inEscherichia coli) as the enzyme sources. A two‐step incubation method was employed to examine thein vitromechanism‐based inactivation (MBI) criteria. Potential metabolite–intermediate complex (MIC) formation was studied by spectral analysis.RESULTSTCAs generally exhibited significant TDI of recombinant CYP1A2, CYP2C19 and CYP2D6 (>10% positive inhibition differences between co‐ and preincubation conditions). TDI of recombinant CYP2C9 was minor (<10%), and was minor or absent in experiments utilizing recombinant CYP3A4 or HLM as the enzyme sources. Where observed, TDI of recombinant CYP occurred via alkylamine MIC formation, but evidence to support similar behaviour in HLM was limited. Indeed, only secondary amine TCAs reduced the apparent P450 content of HLM (3–6%) consistent with complexation. As a representative TCA, nortriptyline fulfilled thein vitroMBI criteria using recombinant CYP2C19 and CYP3A4 (KIandkinactvalues of 4 µmand 0.19 min−1, and 70 µmand 0.06 min−1), but not with the human liver microsomal enzymes.CONCLUSIONSTCAs appear to have minimal potential for MBI of human liver microsomal CYP enzymes involved in drug metabolism. HLM and recombinant CYP (expressed inE. coli) are not equivalent enzyme sources for evaluating the TDI associated with some drugs.
Adverse drug reaction monitoring in a secondary care hospital in South India
Authors: Arulmani R. , Rajendran S.D. , Suresh B. 
Published: July 2007

What is already known about this subject • The benefits of adverse drug reaction (ADR) monitoring are well‐known.• Poor awareness and nonavailability of a central co‐ordinating body resulted in lack of ADR monitoring in India.• The National Pharmacovigilance Programme was recently initiated, encouraging ADR monitoring in selected centres, including our centre. What this study adds • This is the first study of its kind at GHQH, Ootacamund that has provided insight into the burden of ADRs here.• The incidence and severity of ADRs documented in our study is lower than those reported in comparable populations in Western studies but more than those reported in India.AimsTo ascertain the current burden of ADRs at a Government hospital in Ooty and to assess the severity of reported ADRs and the additional financial burden associated with ADRs.MethodsA prospective, spontaneous reporting study was conducted over a period of 9 months of inpatient admissions to the medical wards, co‐ordinated by clinical pharmacists. The WHO definition of an ADR was adopted. The Naranjo algorithm scale was used for causality assessment. Confirmed ADRs were classified according to the Wills & Brown [7] method and assessed for severity and patient outcomes. The average cost incurred in treating the ADRs was calculated.ResultsOf the total of 187 adverse drug events (ADEs) reported, 164 reports from 121 patients were confirmed as ADRs, giving an overall incidence of 9.8%. This included 58 (3.4%) ADR related admissions and 63 (3.7%) ADRs occurring during the hospital stay. About two thirds of the reactions (102, 62.2%) were classified as probable. The majority of the reactions (88, 53.7%) were mild. Most patients (119, 72.6%) recovered from the incidence. The majority of the reactions were of type H (100, 61%) which indicates that they were not predictable and not potentially preventable. An average cost of 481 rupees (£6) was spent on each patient to manage ADRs.ConclusionsThe incidence and severity of ADRs documented in our study are lower than those reported in comparable populations in Western studies but more than those reported in India.