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J Durlach

Publications and source records attributed to J Durlach.

At least 37 records · Page 2Linked to original sources
PubMed1999

Cardiovasoprotective foods and nutrients: possible importance of magnesium intake.

Various highly efficient cardiovasoprotective diets associate reduced intake of total and saturated fats, reasonable supply of monounsaturated fat and omega-3 fatty acids, moderate consumption of alcohol, increased intake of cereals, fruits, vegetables, fish and low fat dairy products. Among several protective nutrients magnesium should be given particular consideration because of the very frequent occurrence of chronic primary magnesium deficiency which appears to act as a cardiovascular risk factor and also reversely, because of the noticeable high level of the magnesium content in cardiovasoprotective diets.

Cardiovascular Diseases↗
PubMed1999

Magnesium pidolate and magnesium aspartate effects on human amniotic membrane ionic permeability in vitro.

The effects of Mg pidolate and Mg aspartate were studied on the ionic transfer through a membraneous model: the human isolated amniotic membrane. The ionic transfer was evaluated by the measure of the total conductance in the maternal to fetal way (GtM) and in the fetal to maternal way (GtF) and of the ionic fluxes (F1 on the maternal side (MS), F2 on the fetal side (FS)) and of the ratio F1/F2. Whatever the Mg pidolate concentration, GtM and GtF remained constant. Mg aspartate had a concentration-dependent effect on GtM (decrease-increase) and a monophasic effect on GtF (decrease). F1 and F2 were decreased by the two Mg salts, and the ratio F1/F2 remained constant after addition of Mg pidolate and was increased by Mg aspartate. The results were explained in terms of screening and/or binding interactions with the polar surface moieties and were compared with results obtained in previous studies with other Mg salts. The results indicated the importance of the anion associated with Mg element in the ionic transfer.

Amnion↗
PubMed1998

Magnesium status and ageing: an update.

Ageing constitutes a risk factor for magnesium deficit. Primary magnesium deficit originates from two etiological mechanisms: deficiency and depletion. Primary magnesium deficiency is due to insufficient magnesium intake. Dietary amounts of magnesium are marginal in the whole population whatever the age. Nutritional deficiencies are more pronounced in institutionalized than in free-living ageing groups. Primary magnesium depletion is due to dysregulation of factors controlling magnesium status: intestinal magnesium hypoabsorption, reduced magnesium bone uptake and mobilisation, sometimes urinary leakage, hyperadrenoglucocorticism by decreased adaptability to stress, insulin-resistance and adrenergic hyporeceptivity. Secondary magnesium deficit in ageing largely results from various pathologies and treatments common to elderly persons: i.e. non insulin dependent diabetes mellitus and use of hypermagnesuric diuretics. Magnesium deficit may participate in the clinical pattern of ageing: mainly neuromuscular, cardiovascular and renal symptomatologies. The consequences of hyperadrenoglucocorticism--whose non response to dexamethasone suppression test appears the simplest marker--may concern immunosuppression, muscle atrophy, centralization of fat mass, osteoporosis, hyperglycemia, hyperlipidemia, atherosclerosis, disturbances in mood and mental performances through accelerated hippocampal ageing particularly. Treatment of magnesium deficiency requires simple oral physiological magnesium supplementation. Treatment of the different types of magnesium depletion leads to a more or less specific control of pathophysiological disturbances of the required magnesium substrate. Open and double blind studies on the effects of the treatments of magnesium deficiency and of magnesium depletions in geriatic populations are too scarce. Further study is necessary to assess the accurate place of magnesium deficit in the physiopathology of ageing.

Age Factors↗
PubMed1998

Comparative experimental study of Mg lactate, vitamin B6 and their association on the permeability of a human membrane. 2. Effects on cellular and paracellular ionic transfer through isolated amniotic membrane.

The comparative effects of Mg lactate, pyridoxine chlorhydrate and their association were observed on the various components of the human transamniotic conductance Gt. The use of both microelectrodes and metabolic inhibitors indicates 12 components of Gt: 8 cellular components Gc (Na-K, ATPase, Na-H and Cl-HCO3 antiports, Na-K-2Cl cotransport, Na-Mg exchanger and Na, K, Cl channels), one coupling component and three paracellular components Gp (Na, K, Cl). Mg lactate had a monophasic action on some components (decrease or increase conductance), according to its concentration, on maternal side (MS): GpNa, GpK, GpCl, K channels, conductance due to Na-K, ATPase. On fetal side (FS), there is a monophasic action on GpK, Na channels and a biphasic action (decrease then increase conductance) on GpNa and Na/Mg (as on MS). Pyridoxine chlorhydrate had a monophasic action on GpNa (MS, FS), GpK (MS), Na/Mg (MS, FS) and a biphasic action on GpK (FS), Na channels (MS, FS). The association of both Mg lactate and pyridoxine chlorhydrate implicated a biphasic action on all cationic components on both sides (GpNa, GpK, Na and K channels, Na/H, Na-K-2Cl, Na/Mg. The anionic components were not modified with regard to agents. The Mg lactate + vitamin B6 association interferes specifically with the cationic conductance components with regard to individual components.

Amnion↗
PubMed1997

Stability of brain content of magnesium in experimental hypomagnesemia.

Magnesium is important in cerebral function. If there is a deficiency and neurological symptoms accrue, we hypothesised that Mg2+ deficiency causes neurological symptoms by decreasing the level of Mg2+ in cerebral tissue. The content of magnesium was determined in 12 brain structures in magnesium-deficient rats. Experiments were carried out for 40 days in two groups of Wistar male rats made magnesium-deficient (MD) by a well-controlled diet (50 mg of Mg2+/kg of food), and a control group (CG) rats fed normal diet (1 g of Mg2+/kg of food). At the end of the 40 days, the clinical signs of hypomagnesemia were sought in the MD rats and Mg2+ concentration levels were measured in the blood and brain. The results showed variable distribution of Mg2+ in the different brain structures, both in CG and MD rats; in the MD rats there is an important stability of global Mg2+ content of the brain. Although the global values for Mg2+ in the brain did not decline in MD rats, there was a significant decrease in Mg2+ in the brainstem. We conclude that the brain is able to maintain a stable concentration of Mg2+ during chronic hypomagnesemia, but its topographic variations could account for some of neurological signs accompanying this condition.

Animals↗
PubMed1997

Neurotic, neuromuscular and autonomic nervous form of magnesium imbalance.

The nervous form of magnesium imbalance represents the best documented experimental and clinical aspects of magnesium disorders. The nervous form of primary magnesium deficit (MD) in the adult appears as the best descriptive model for analysis of the symptomatology, aetiology, physiopathology, diagnosis and therapy of the most frequent form of MD. Nervous hyperexcitability due to chronic MD in the adult results in a non-specific clinical pattern with associated central and peripheral neuromuscular symptoms, analogous to the symptomatology previously described in medical literature as latent tetany, hyperventilation syndrome, spasmophilia, chronic fatigue syndrome, neurocirculatory asthenia and idiopathic Barlow's disease. On encountering this non-specific pattern, the signs of neuromuscular hyperexcitability are of much greater importance. Trousseau's sign is less sensitive than Chvostek's sign, but their sensitivities are increased by hyperventilation (Von Bondsdorff's test). Examination of the precordial area will be conducted in order to search clinical stigmata of mitral valve prolapse (MVP) which is a frequent dyskinesia due to chronic MD (about a quarter to one-third of cases). The electromyogram (EMG) shows one (or several) trains of autorhythmic activities beating for more than 2 min of one of the three tetanic activities (uniplets, multiplets or 'complex tonicoclonic tracings') during one of the three facilitation procedures: tourniquet-induced ischaemia lasting 10 min. post-ischaemia lasting 10 min after the removal of the tourniquet and hyperventilation over 5 min. A repetitive EMG constitutes the principal mark of nervous hyperexcitability (NHE) due to MD. The echocardiogram (ECC) is the best tool for detecting MVP, the 2-dimensional ECC with pulsed Doppler being more accurate than time-motion ECC. The routine ionic investigations comprise five static tests: plasma and erythrocyte magnesium, plasma calcium and daily magnesiuria and calciuria. An evaluation of magnesium intake is desirable. Normal concentrations of magnesium in blood do not rule out the diagnosis of the nervous form of primary chronic MD. The histograms of MD group reveal Gaussian type magnesaemias with significantly lower means and the constituent elements can be individually hypo- (one-third of cases), normo- (about two-thirds of cases) and even, exceptionally, hyper-magnesaemic. The diagnosis of MD requires an oral magnesium load test. At physiological dose (5 mg of Mg/kg/day), oral magnesium is totally devoid of the pharmacological effects of parenteral magnesium. Corrections of symptomatology by this oral physiological magnesium load is the best proof that it was due to magnesium deficiency. In particular clinical forms, more sophisticated studies may be useful: standard and quantitative electroencephalograms, electropolygraphic studies of afternoon sleep, electronystagmography, optokinetic test, skin conductance reflex, psychometric inventories, standard or monitoring electrocardiogram, treadmill test, other static and dynamic investigations: e.g. ionized free Mg2+, lymphocyte Mg, brain Mg, cerebrospinal Mg, Mg balance, Mg parenteral load test, glucose load, and even radio-isotope study, the only one able to reveal intestinal magnesium hypersecretion. Nervous primary chronic MD progresses by phases of decompensation against a background of latency. Marginal magnesium deficiency, that is to say an insufficient magnesium intake which merely requires simple oral physiological supplementation, is fundamental in the aetiology of primary magnesium deficit. However a constitutional homeostatic lability of the nervous system or of magnesium metabolism such as belonging to the B35 type of HLA group must be involved. Part of the aetiology of this magnesium deficit is a magnesium depletion, where the disorder which induces magnesium deficit is related to a dysregulation of the control mechanisms of magnesium status which requires a more or less difficult

Administration, Oral↗
PubMed1997

Comparative experimental study of Mg lactate, vitamin B6 and their association on the permeability of a human membrane. 1. Effect on the total ionic transfer through isolated amniotic membrane.

The effects of Mg lactate, vitamin B6 and their association were studied on the ionic transfer through a membranous model: the human isolated amniotic membrane. The ionic transfer was evaluated by measuring of the total conductance in the maternal to fetal way (GtM) and in the fetal to maternal way (GtF) and of the ionic fluxes (F1 on the maternal side, F2 on the fetal side) and of the ratio F1/F2. Whatever the concentration, Mg lactate decreased GtM, F1, F2, F1/F2 but had a concentration-dependent effect on GtF. Vitamin B6 had no significant effect on GtF, F1, F2, F1/F2, but decreased GtM whatever its concentration. The association Mg lactate + vitamin B6 presented a biphasic action on GtM, GtF, F1, F2 and F1/F2: decrease at low ratio and increase from ratio equal to 8. This association induced interesting effect in the case of therapeutic use in comparison with the effects of separated compounds.

Amnion↗
PubMed1997

Are age-related neurodegenerative diseases linked with various types of magnesium depletion?

Age-related human neurodegenerative diseases are a major social and medical problem. It is therefore logical to take into consideration every theory with an overall approach to neurodegenerative diseases. This environmental proposal relies mainly on data concerning the Western Pacific amyotrophic lateral sclerosis-Parkinsonism-dementia complex (WP ALS-PD) considered as 'a prototypal human neurodegenerative disease' and on extrapolation from it to the bulk of neurodegenerative diseases (NDD). NDD would be due to an accelerated ageing process in certain populations of neurons due to the noxious synergy of (1) increased environmental slow deleterious factors (such as slow toxins) and of (2) decreased environmental protective factors (Mg deficient intake particularly). First, it was observed that three apparently dissimilar conditions occurred at extraordinary high rates in the Guam area: motoneuron disease (ALS), Parkinson's disease (P) and Alzheimer's-like dementia (D). Next, several other foci of endemic ALS-PD were found in Asia and Oceania in three Western Pacific population groups. These included the Chamorro people in Mariana Islands (Guam and Rota), the Auyu and Jakai people of West New Guinea and the Japanese residents of the Kii peninsula (Honshu island). The post-Second World War decline of the occurrence of WP ALS-PD in all three high incidence disease foci coupled with the absence of demonstrable heritable or transmissible factors had led to focus the search for the cause of this degenerative disease on nontransmissible environmental factors that are disappearing as the susceptible population groups acculturate to modern way. Epidemiologic study has shown that preference for traditional Chamorro food is the only one of 23 tested variables significantly associated with an increased risk for PD. An early suggestion incriminated the toxic seed of the false sago palm (Cycas circinalis L) which was used in traditional food and medicine. Laboratory investigation of cycad seed revealed the presence of various toxins and particularly of an 'unusual' non protein aminoacid: L-BMAA (beta-N-methylamino-L-alanine), an excitotoxic aminoacid. This slow toxin presents some structural similarity to another 'unusual' excitotoxic aminoacid: L-BOAA (beta-N-oxalyl-amino-L-alanine), an exogenous neurotoxin present in the grass pea (Lathyrus sativus) whose excessive consumption may cause lathyrism. The excitotoxicity of both L-BMAA and L-BOAA mainly concerns non-NMDA receptors. The neurotoxicity of these aminoacids varies with experimental models failing to induce an experimental model akin to WP ALS-PD or displaying many of the motor-system and behavioral changes of WP ALS-PD. It may be due to the presence of physiological levels of bicarbonate or of various toxic cofactors: bio-organic such as cycasin or inorganic such as pollutant metals e.g. aluminum or manganese, together with the lack of protective factors (e.g. calcium and magnesium deficiencies). Combined Al intoxication with Ca-Mg deficiencies is a reasonable model to investigate the pathogenesis of neurodegenerative diseases and eventually to screen their treatments. It may also be considered as a model of magnesium deficit, but it does not concern simple magnesium deficiency reversible with mere oral physiological magnesium supplementation. Magnesium deficiency cannot result in neurodegenerative disease. Combined Al intoxication with Ca-Mg deficiencies is not reversible through physiological oral magnesium supplementation. It therefore constitutes a type of experimental magnesium depletion model, instrumental in the investigation of the pathogenesis of magnesium depletion and in the screening of its still unknown possible treatments. (ABSTRACT TRUNCATED)

Aging↗
PubMed1996

Reversible model of magnesium depletion induced by systemic kainic acid injection in magnesium-deficient rats: I--Comparative study of various magnesium salts.

We developed three models of reversible magnesium depletion in rats resulting from the combined effects of kainic (KA) acid with magnesium deficiency, in order to compare the effects of various common magnesium salts (pidolate, aspartate, lactate, gluconate and chloride) and of magnesium acetyl taurinate (MgATa), administered daily (14 mg Mg2+, PO) for ten days. First, the immediate effects (wet dog shakes, clonic convulsions and death 1 h after injection) and late effects (fall from hole board between the second and tenth days post injection) of kainic acid at three different doses (3.6 and 11 mg/kg) were studied in magnesium deficient rats (50 ppm for 40 days) and in non-deficient rats (1700 ppm). The results showed that the effects of kainic acid were enhanced in magnesium deficient rats. Secondly, after ten days of physiological then pharmacological doses of magnesium, used as chronical supplementation, we showed that kainic acid administration combined with magnesium deficiency led to magnesium depletion of increasing severity depending on the dose of kainic acid. The observed magnesium depletions were weak at a dose of 3 mg/kg KA, moderate at a dose of 6 mg/kg and severe at a dose of 11 mg/kg. These depletions were more or less reversible, and this enabled the classification of the therapeutic effects of these salts on Mg depletion. Among common salts, magnesium pidolate presented the greatest efficacy but none of them fully prevented depletion. In contrast, MgATa was efficient on all the aspects of depletion, when administered preventively both chronically or acutely or as a single curative injection. Consequently the results we obtained in the present study, on a new model of magnesium depletion, showed the greatest efficacy of magnesium acetyl taurinate we demonstrated yet on other models of reversible magnesium depletion.

Administration, Oral↗
PubMed1995

Comparative studies of Ca N-acetylhomotaurinate and Ca N-acetyltaurinate. I. Effects on the ionic transfer through the isolated human amnion.

The effects of two taurine and homotaurine derivatives (Ca N-acetyltaurinate: ATACa and Ca N-acetylhomotaurinate: AOTACa) were studied on the ionic transfer through a membranous model: the human isolated amniotic membrane. The ionic transfer was evaluated by measurements of the various components (cellular and paracellular) of the total conductance across the membrane. AOTACa influenced all the components of the total ionic conductance without flux ratio modifications and the general action scheme was a biphasic effect: decrease conductance with low concentrations and increase conductance with high concentrations. This effect might be important in the case of lower or higher supplementation. ATACa only interfered with some conductance components and this action was predominantly monophasic (decreased or increased conductance). This study indicates differential actions between two closely related molecules on a membranous model.

Acamprosate↗
PubMed1995

Red blood cell magnesium concentrations: analytical problems and significance.

In order to assess total magnesium concentrations in human red blood cells (erythrocytes--ErMg), atomic absorption spectrometry (AAS) provides high accuracy and precise method rapid and amenable to automation. Taking care of eliminating the chronic marginal magnesium deficits, normal values of ErMg evaluated through a direct method and expressed as mmol/litre of packed cells are 2.3 +/- 0.24. Inductively coupled plasma-mass spectromettry (ICP-MS) is a multielemental analytical technique. Particle induced x-ray emission (PIXE) also provides multielemental capability, but is time-consuming and costly. Microelectrodes are the gold standard for intracellular Mg2+ measurements. But microelectrodes and fluorescence probes measure the activity of magnesium ions, not the concentrations. Ionized magnesium content of human intact erythrocyte is mainly assessed with the NMR method and with the zero point titration. The concentration of ionized magnesium as estimated by NMR (31P NMR method) was found to be 0.20 +/- 0.02 mmol/litre cell water and with the zero point titration 0.55 +/- 0.12. The uncertainty concerning the two current used techniques for free magnesium determination is worsened by the fact that magnesium inside red cells continually oscillates in vivo. Free magnesium constitutes a small part of total magnesium. Further studies are necessary to assess the importance of its variations in clinical medicine. Efflux of ErMg is controlled through membranous sodium-dependent and sodium-independent pathways and through genetic and neurohormonal regulations. Variations in the total or ionized ErMg do not necessarily mean that similar changes should exist in the magnesium pool. But it remains the basic static cellular magnesium item. Its value will be subsequently enhanced when it takes place among the clinical and paraclinical data of dynamic magnesium investigations.

Blood Chemical Analysis↗
PubMed1995

Editorial policy of Magnesium Research: general considerations on the quality criteria for biomedical papers and some complementary guidelines for the contributors of Magnesium Research. Society for the Development on Magnesium Research.

The quality criteria of biomedical journals--and of 'Magnesium Research' as such--are being given a new insight. This has practical implications for the contributors and the editors. General considerations on the patterns of evaluation of scientific papers highlight five types of errors, that may be incurred in submitted manuscripts. 1. The information conveyed may remain ambiguous: for example, lack of discrimination between acute and chronic patterns, or confusion between the clinical and toxicological consequences of pharmacological and physiological studies: for example it is a real scientific fraud to identify the absent toxic effects of physiological magnesium supplementation with those of high pharmacological magnesium doses ... which in fact may induce toxicity. There should be no confusion between in vitro and in vivo data, with a good understanding of the systemic neuroendocrine metabolic and renal regulations and of the multiple local targets concerned. It is always important to discriminate between the two types of deficit: deficiency due to insufficient intake which merely requires oral physiological supplements and depletion related to a dysregulation which requires more or less specific correction of its causal dysregulation. 2. Insufficient information retrieval, frequently with consultation of one data-base only. Because of indexing omissions and word usage idiosyncrasies, no literature search can retrieve all papers. Monographs and books of proceedings are rarely mentioned in databases and therefore escape consultation. It is obvious, besides, that some of the quoted references have sometimes not been read, but only the title (and in the best cases also the abstract), occasionally with the remaining misprints. A good specific and general knowledge of the background of the study is necessary. 3. Basic methodological errors. Coexistence does not mean causality. Analogous patterns do not demonstrate an identical aetiopathogenesis. The complexity of biology must not be disregarded just because the present trend focuses on one aspect of knowledge at the expense of many others. 4. Thought processes must be unbiased. Citation of supportive papers to the prejudice of unsupportive papers constitutes a real ethical fraud. It seems also very important to submit for publication papers with negative results as well as ones with positive results. In studies on pharmacological indications for magnesium, choice of the magnesium salt used ought to be justified and the efficiency must be evaluated vs reference treatment. 5. Observance of the formal regulations is frequently neglected, in the presentation of manuscripts particularly. Some guidelines should therefore be added to the directions to contributors. Before establishing valuable protocols and in order to write up well structured introductions, discussions and conclusions, the authors should have a comprehensive view of their subjects, that is to say an overall knowledge of the previous general and specific publications related to the topic which must be read. Title, conclusions and abstract ought to be taken into account in the discussion. References should be duly consulted or mentioned as 'cited in'. There should be strict observance of the presentation of the manuscripts according to the directions to contributors. Studies resulting in negative results should not be disregarded. Reciprocally, the editorial policy requires that editors and referees ought to be strict as regards the quality criteria. Although editors and peer reviewers are in no position to detect basic fraud they can, however, highlight errors, whether due to simple oversight or to more subtle ethical or scientific pseudo-frauds. Both conclusive and inconcern papers may deserve publication: positive and negative results equally concern public health. To conclude, the editorial board must be ready to reject dubious manuscripts but must at the same time keep their minds open to consider in a positive l

Animals↗