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Biomedical subjects

L Beck

Publications and source records attributed to L Beck.

At least 19 recordsLinked to original sources
PubMed2006

[Evaluation of a formula with low protein content and supplemented with probiotic agents after breast milk weaning].

UNLABELLED: Besides assuring growth and development in early infancy, human breast milk plays a key role in preventing infections, in particular by favouring the growth of bifidobacteria. The development of infant formulas containing probiotic agents consequently represents a significant advance in the provision of an optimal alternative to breast feeding when this is not feasible. A further concern is to avoid an excessively high protein content relative to breast milk, potentially favouring obesity in later life. OBJECTIVES: The objective of this open Multicenter comparative study was to demonstrate that a new infant formula, characterized by a reduced protein content and the presence of a probiotic agent, was as effective as conventional formulas in assuring growth during the first months of life. POPULATION AND METHODS: The study population comprised full-term healthy infants with an age at inclusion of 1-28 days, whose mothers no longer wished to continue breast feeding or were unable to breast feed. The test formula (GE), enriched with Bifidobacterium lactis, had a protein content of 1.5 g/100 ml. The primary end point was daily weight gain from day 0 to day 90. Secondary end points were daily increase in height and cranial circumference, overall and gastrointestinal tolerance and formula acceptability. A total of 203 infants were included in the analysis, 117 receiving GE and 86 the formula habitually prescribed by the paediatrician. RESULTS: Daily gains in weight, height and cranial circumference did not differ significantly between the groups. The rates of overall and gastrointestinal adverse events were comparable in the two groups and the acceptability of GE was consistently good, similar to that of the standard formulas. CONCLUSION: The results of this study demonstrated that the new probiotic infant formula GE has equivalent efficacy to conventional formulas in achieving growth in early infancy, and is well tolerated.

Bifidobacterium↗
PubMed2006

Reproducibility of automated pulse wave velocity measurement during exercise. Running head: pulse wave velocity during exercise.

Pulse wave velocity measurement is used as an index of arterial stiffness. The purpose was to evaluate the reproducibility of pulse wave velocity measurement at rest, during exercise and recovery from exercise, using an automated device. Twelve healthy young adults (mean age 22.0 +/- 3.1 yrs) underwent an upright submaximal cycle test on two separate occasions, one week apart. Pulse wave velocity, systolic and diastolic blood pressures and heart rate were assessed at rest, during the last 2 min of exercise and 10 min later. Pulse wave velocity was measured on the upper limb and the forearm by the cross-correlation function of photoplethysmography and Doppler signals. Brachial artery pulse wave velocity was calculated from upper limb and forearm pulse wave velocities. No significant difference was found on duplicate measurements of heart rate, systolic and diastolic blood pressures at rest, during exercise and recovery, showing that pulse wave velocity was measured under similar conditions. Coefficient of variation for upper limb and forearm pulse wave velocities ranged from 2.9 to 5.9% at rest and during recovery, and were respectively 2.9% and 8.3% during exercise. However, coefficient of variation for brachial pulse wave velocity was 7.7 and 10.3% at rest, 15.7% during exercise, and 5.8% during recovery. During exercise, pulse wave velocity measurements were satisfying, but indirect assessment of brachial artery pulse wave velocity showed poor reproducibility. Thus, upper limb and forearm pulse wave velocities may be used during exercise to assess the effect of training or drugs on arterial wall mechanical properties.

Adult↗
PubMed2005

Effect of intensive training on heart rate variability in prepubertal swimmers.

BACKGROUND: In children, there is very limited evidence focusing on the beneficial effect of exercise training on heart rate variability (HRV) during childhood. Despite the fact that more and more children are engaged in intensive training programs, the question arises if such intensive training involves deleterious effects on the cardiac autonomic nervous system during childhood. Thus the aim of the present study was to compare HRV parameters in highly trained swimmer boys and untrained counterparts. METHODS: Twenty prepubertal boys, aged 11-12 years old, took part in the study. The children were divided into 11 highly trained prepubertal swimmers (training sessions of 8-10 h weekly for at least 4 years) and 9 age-matched active boys. HRV analysis was performed on diurnal recordings in the frequency (short-term recordings 6 min the most 'vagal') and time (long-term recordings 4 h centred on the 6 min most 'vagal') domains. RESULTS: No significant differences were obtained between groups for all frequency variables whatever the mode of expression (absolute in ms2, relative in Ln or %). All time-domain components were not significantly different in swimmers and untrained boys. CONCLUSIONS: The results of the present study demonstrate that participating intensively in swimming training does not induce in children changes in HRV indices. Neither time nor domain HRV variables were significantly different between untrained and highly trained prepubertal boys. Thus, intensive training in healthy children does not involve deleterious effects on HRV.

Child↗
PubMed2004

[Pharmacological treatment of atrial fibrillation].

Although anticoagulant treatment of atrial fibrillation is now well codified, the medical treatment of the fibrillation remains controversial. Two types of medication can be proposed: drugs to slow the rhythm (digitalis, betablockers and calcium inhibitors) and anti-arrhythmic mainly Class I or Class III drugs. Some doubt was raised in the 1990's about the pertinence of antiarrhythmic therapy and four recent trials (AFFIRM, RACE, PIAF and STAF) compared the two attitudes of "rhythm control" or "rate control" in atrial fibrillation. The four trials all showed that the results of these two options were equivalent with respect to the therapeutic objectives: reduction of mortality, thromboembolic or haemodynamic risk, and regression of symptoms and improvement of the quality of life. However, these trials have not closed the debate on these two therapeutic attitudes. In fact, analysis shows that the comparison was biased because anticoagulant treatment was inadequate and, though the treatment for rate control was appropriate, the antiarrhythmic treatment was far from being satisfactory and effective. Moreover, many patients in the "rhythm control" group were in atrial fibrillation whereas a certain number of patients in the "rate control" group were, in fact, in sinus rhythm throughout the study period. In addition, the comparison was incomplete because it did not include two other particularly common populations in clinical practice: multi-relapsing paroxysmal atrial fibrillation in healthy hearts and atrial fibrillation associated with severe left ventricular dysfunction, patients with cardiac failure. Until the results of trials currently under way (AF-CHF) become available, the authors discuss the use of drugs for rate control and antiarrhythmic therapy in everyday practice.

Adrenergic beta-Antagonists↗
PubMed2003

[Mechanisms of action of antiarrhythmics in cardioversion of atrial fibrillation and atrial flutter].

The mechanisms of action of antiarrhythmic drugs at atrial level are multiple. Antiarrhythmics may act at three levels in the prevention of paroxysmal atrial fibrillation: on the arrhythmogenic atrial substrate, the initiating extrasystoles including those of the pulmonary veins, and in the modulation of the autonomic nervous system. However, there are many modes of initiation which are not well understood so that the preventive role of the antiarrhythmic drugs remains imprecise. Cardioversion of persistent atrial fibrillation has been better analysed in healthy hearts: Class I antiarrhythmics in particular, despite their depressive effects on the conduction which are potentially arrhythmogenic, are beneficial by decreasing the number of reentry circuits, prolonging the atrial refractory period on short cycles and, paradoxically, by increasing the period of excitability in AF. All have a preferential action on anisotropic conduction, especially at the pivotal point of reentry. On the other hand, their role in electrophysiological remodelling in the prevention of immediate recurrences and in pathological atria, remains poorly understood. As for atrial flutter, despite many clinical and experimental studies with antiarrhythmics, the current predominant role of radiofrequency ablation greatly limits the value of these pharmacological studies.

Anti-Arrhythmia Agents↗
PubMed2003

[Arrhythmogenic effects of non cardiovascular drugs].

Among the unwanted effects of drugs, arrhythmogenic effects are particularly fearsome. Although rare they are serious, and responsible for syncope or sudden death, often linked with torsades de pointe on established long QT. For non cardiovascular drugs, detection is difficult because patients do not undergo systematic cardiological surveillance. Nevertheless understanding the risk, identification of predisposing factors, and consideration of the contra-indications are the rules of prescription, which are even more indispensable when the pathology being treated is benign. In effect, the implicated drugs are mainly anti-histamines, antibiotics, neuroleptics and antidepressants. The pharmaceutical companies, regulatory agencies, and pharmacological surveillance services must recognise the greatest possible risk of a drug, thanks to pre-clinical data, experimental electrophysiology both in vivo (measurement of the QT interval) and in vitro (action potential duration) or even in the elementary channel (essentially analysis of the iKr current). Correlated with clinical data (QT changes, pharmacokinetic interactions), a risk/benefit profile can therefore be established, which is even more demanding when the pathology is benign or when alternative drugs are available.

Arrhythmias, Cardiac↗
PubMed2002

[Monophasic action potentials: considerations and limits].

Monophasic action potentials are currents recorded in vivo in the extracellular milieu which can reproduce the repolarisation signal of intracellular action potentials. For a long time unstable and complex to record, they now require simply a firm myocardial contact with a bipolar electrophysiological catheter and modification with recording filters, without a high-pass filter (DC). They have been widely used in recent years to study in vivo modifications of the action potential durations with frequency, epi-, endo-, or intramyocardial cellular topography, endocavity pressure modifications, or antiarrhythmic medication. They allow a unique means of continuous analysis in animals or in patients of the action potentials during polymorphic arrhythmias such as atrial fibrillation, ventricular fibrillation and torsades de pointes, although in these cases the refractory periods can not be measured precisely and continuously, beat after beat. In contrast, their clinical or experimental use in the study of arrhythmias dependent on premature post-depolarisations has without doubt been excessive and disputable, because it appears improbable that authentic premature post-depolarisations could ever be obtained on a monophasic action potential, which always represents the summation of the action potentials of dozens of cells.

Action Potentials↗
PubMed2001

Contact lens-associated chemical burn.

We present the case of a young man who presented as an ophthalmic casualty after inserting a pair of bizarre-effect cosmetic hydrogel contact lenses while in a night-club. He failed to follow the manufacturer's guidelines and inserted the lenses before neutralising the storage solution. On presentation he was found to have bilateral corneal epithelial defects which required hospital treatment for 4 days. He appears to have suffered no long-term sequelae.

Journal Article↗
PubMed2001

Molecular aspects of renal tubular handling and regulation of inorganic sulfate.

The renal proximal tubular reabsorption of sulfate plays an important role in the maintenance of sulfate homeostasis. Two different renal sulfate transport systems have been identified and characterized at the molecular level in the past few years: NaSi-1 and Sat-1. NaSi-1 belongs to a Na(+)-coupled transporter family comprising the Na(+)-dicarboxylate transporters and the recently characterized SUT1 sulfate transporter. NaSi-1 is a Na(+)-sulfate cotransporter located exclusively in the brush border membrane of renal proximal tubular and ileal cells. Recently, NaSi-1 was shown to be regulated at the protein and mRNA level by a number of factors, such as vitamin D, dietary sulfate, glucocorticoids and thyroid hormones, which are known to modulate sulfate reabsorption in vivo. The second member of renal sulfate transporters, denoted Sat-1, belongs to a family of Na+-independent sulfate transporter family comprising the DTDST, DRA and PDS genes. Sat-1 is a sulfate/bicarbonate-oxalate exchanger located at the basolateral membrane of proximal tubular epithelial cells and canalicular surface of hepatic cells. Contrary to NaSi-1, no physiological factor has been found to date to regulate Sat-1 gene expression. Both NaSi-1 and Sat-1 transporter activities are implicated in pathophysiological states such as heavy metal intoxication and chronic renal failure. This review focuses on recent developments in the molecular characterization of NaSi-1 and Sat-1 and the mechanisms involved in their regulation.

Amino Acid Sequence↗
PubMed2001

Effects of spironolactone and fosinopril on the spontaneous and chronic ventricular arrhythmias in a rat model of myocardial infarction.

We documented chronic ventricular arrhythmias in a first group of 58 rats after myocardial infarction (MI), then assessed the effects of spironolactone and fosinopril on morphological indexes and arrhythmias in a second group (n = 33). Rats underwent Holter monitoring at 2 months after MI. Treatment was randomly given from 1 until 4 months after MI: placebo in 12 rats (P), fosinopril in 9 (F) and spironolactone + fosinopril in 12 (SF). The score of ventricular premature beats (VPBs) was related to the MI size and the delay from MI (p < 0.01). VPB's reduction/increase required to demonstrate anti/pro-arrhythmic effects were 55 and 59%. Mass indexes were lower in F and SF (p = 0.01). VPB's difference (4 months vs. 1) was positive in P, significantly lower in F and negative in SF (p = 0.04). In this relevant model of spontaneous and chronic ventricular arrhythmias, SF association did not increase mortality but lowered the arrhythmic score.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2001

Replacing oxamniquine by praziquantel against Schistosoma mansoni infection in a rural community from the sugar-cane zone of Northeast Brazil: an epidemiological follow-up.

A group of 52 villagers was followed-up for three years regarding Schistosoma mansoni infection. All villagers were periodically surveyed by the Kato-Katz method. In March 1997 and March 1998 the positives were treated with oxamniquine (15-20 mg/kg), and in March 1999, with praziquantel (60 mg/kg). All infection indices decreased substantially between March 1999 and March 2000: prevalence of infection (from 32.7% to 21.2%), prevalence of moderate/heavy infection (from 7.7% to 1.9%), intensity of infection (from 23.1 epg to 7.4 epg) and reinfection (from 35.7% to 14.3%). Negativation increased from 53.8 to 82.4. An optimistic prognostic is assumed in the short term for the introduction of praziquantel in the study area.

Animals↗
PubMed2001

[Electrocardiographic alternans].

A simple ECG curiosity or a precursor of serious arrhythmia, associated with pericardial effusion or a sign of inotropic alteration, the phenomenon of electrical alternans has intrigued clinicians and research workers in its multiple facets, mechanical and electrical, consequences on PR interval, QRS complex or ventricular repolarisation. As a consequence, the causal mechanisms are very different, but these last few years, a predominant role of calcium flux, especially intracellular, has been demonstrated. Recently, clinical interest in this phenomenon has been revived with the demonstration of micro-alternans of repolarisation, apparently a new marker for the risk of sudden death.

Arrhythmias, Cardiac↗
PubMed2001

[Molecular aspects of phosphate homeostasis in mammals].

Renal phosphate reabsorption, the major determinant of phosphate homeostasis, is primarily dependent on dietary phosphate content and multiple hormonal factors. Over the last few years, the identification of sodium-dependent phosphate transporters in kidney, intestine and bone, as well as new insights into the molecular mechanisms involved in several hereditary hypophosphatemias, allow to set up novel phosphate reabsorption regulatory pathways. This review describes molecular players involved in these mechanisms, summarizes phosphate transport data in kidney, intestine and bone, and describes recent findings concerning the three most common hereditary hypophosphatemias.

Absorption↗
PubMed2000

The human renal sodium sulfate cotransporter (SLC13A1; hNaSi-1) cDNA and gene: organization, chromosomal localization, and functional characterization.

Sulfate plays an essential role during growth, development, bone/cartilage formation, and cellular metabolism. In this study, we have determined the structure of the human Na+-sulfate cotransporter (hNaSi-1) cDNA (Human Genome Nomenclature Committee-approved symbol SLC13A1) and gene (NAS1). hNaSi-1 encodes a protein of 595 amino acids with 13 putative transmembrane domains. hNaSi-1 mRNA expression was exclusive to the human kidney. Expression of hNaSi-1 protein in Xenopus oocytes demonstrated a high-affinity Na+-sulfate cotransporter that was inhibited by selenate, thiosulfate, molybdate, tungstate, citrate, and succinate. Antisense inhibition experiments suggest hNaSi-1 to represent the major Na+-sulfate cotransporter in the human kidney. NAS1 was localized on human chromosome 7, mapped to 7q31-q32, near the sulfate transporter genes, DRA and SUT-1. The NAS1 gene contains 15 exons, spanning over 83 kb in length. Knowledge of the structure, function, and chromosomal localization of hNaSi-1 will permit the screening of NAS1 mutations in humans with disorders in renal sulfate reabsorption and homeostasis.

Amino Acid Sequence↗
PubMed2000

The mouse Na(+)-sulfate cotransporter gene Nas1. Cloning, tissue distribution, gene structure, chromosomal assignment, and transcriptional regulation by vitamin D.

NaSi-1 is a Na(+)-sulfate cotransporter expressed on the apical membrane of the renal proximal tubule and plays an important role in sulfate reabsorption. To understand the molecular mechanisms that mediate the regulation of NaSi-1, we have isolated and characterized the mouse NaSi-1 cDNA (mNaSi-1), gene (Nas1), and promoter region and determined Nas1 chromosomal localization. The mNaSi-1 cDNA encodes a protein of 594 amino acids with 13 putative transmembrane segments, inducing high affinity Na(+)-dependent transport of sulfate in Xenopus oocytes. Three different mNaSi-1 transcripts derived from alternative polyadenylation and splicing were identified in kidney and intestine. The Nas1 gene is a single copy gene comprising 15 exons spread over 75 kilobase pairs that maps to mouse chromosome 6. Transcription initiation occurs from a single site, 29 base pairs downstream to a TATA box-like sequence. The promoter is AT-rich (61%), contains a number of well characterized cis-acting elements, and can drive basal transcriptional activity in opossum kidney cells but not in COS-1 or NIH3T3 cells. We demonstrated that 1,25-dihydroxyvitamin D(3) stimulated the transcriptional activity of the Nas1 promoter in transiently transfected opossum kidney cells. This study represents the first characterization of the genomic organization of a Na(+)-sulfate cotransporter gene. It also provides the basis for a detailed analysis of Nas1 gene regulation and the tools required for assessing Nas1 role in sulfate homeostasis using targeted gene manipulation in mice.

Amino Acid Sequence↗
PubMed2000

Climate and infectious disease: use of remote sensing for detection of Vibrio cholerae by indirect measurement.

It has long been known that cholera outbreaks can be initiated when Vibrio cholerae, the bacterium that causes cholera, is present in drinking water in sufficient numbers to constitute an infective dose, if ingested by humans. Outbreaks associated with drinking or bathing in unpurified river or brackish water may directly or indirectly depend on such conditions as water temperature, nutrient concentration, and plankton production that may be favorable for growth and reproduction of the bacterium. Although these environmental parameters have routinely been measured by using water samples collected aboard research ships, the available data sets are sparse and infrequent. Furthermore, shipboard data acquisition is both expensive and time-consuming. Interpolation to regional scales can also be problematic. Although the bacterium, V. cholerae, cannot be sensed directly, remotely sensed data can be used to infer its presence. In the study reported here, satellite data were used to monitor the timing and spread of cholera. Public domain remote sensing data for the Bay of Bengal were compared directly with cholera case data collected in Bangladesh from 1992-1995. The remote sensing data included sea surface temperature and sea surface height. It was discovered that sea surface temperature shows an annual cycle similar to the cholera case data. Sea surface height may be an indicator of incursion of plankton-laden water inland, e.g., tidal rivers, because it was also found to be correlated with cholera outbreaks. The extensive studies accomplished during the past 25 years, confirming the hypothesis that V. cholerae is autochthonous to the aquatic environment and is a commensal of zooplankton, i.e., copepods, when combined with the findings of the satellite data analyses, provide strong evidence that cholera epidemics are climate-linked.

Bangladesh↗
PubMed2000

Systemic or mucosal administration of immunostimulatory DNA inhibits early and late phases of murine allergic conjunctivitis.

Seasonal allergic conjunctivitis is one of the most common manifestations of allergic disease, affecting 15 % population in the United States annually. Short ragweed (RW) is a major cause of seasonal allergies. Immunostimulatory DNA sequences (ISS or CpG motifs) can inhibit an on-going Th2/allergic response and induce a de novo Th1 response. In this study, we investigated the ability of these ISS to modulate allergic responses in a RW-induced mouse model of seasonal allergic conjunctivitis. Systemic or mucosal administration of ISS oligonucleotide (ISS-ODN) after RW sensitization inhibited both the immediate hypersensitivity response and the late-phase cellular infiltration and induced a RW-specific Th1 response. ISS-ODN administration suppressed the rise of RW-specific IgE titers after repeated allergen challenge. Furthermore, ISS administration was more effective than dexamethasone in inhibiting the allergic response. Mechanistically, the ISS-induced immunomodulatory effects were abolished when mice were treated with anti-IL-12 neutralizing antibodies, suggesting a pivotal role for type 1 cytokines in the inhibition of both the immediate hypersensitivity and the late-phase cellular infiltration. Thus, ISS-ODN is a novel anti-inflammatory and immunomodulatory agent that significantly inhibits the allergic response and may provide an alternative to the current standard care of ocular allergy.

Administration, Topical↗