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J Emmerich

Publications and source records attributed to J Emmerich.

At least 127 records · Page 7Linked to original sources
PubMed1994

[Effects of an educational campaign on cardiovascular risk factors in a French town (Epernon, study town). Methods and preliminary results: prevalence and level of risk factors].

The authors report the methods and preliminary findings of a study scheduled to last 5 years, which aims to evaluate cardiovascular risk factor changes in response to an education program. The population sample consisted of 961 subjects, from Epernon itself (the study town) and from two control towns. The assessment criteria were reported at the beginning of the study and then again after 2 and 5 years. They consisted of an analysis of medical events and of biomedical and dietary data and a detailed analysis of behavior with regard to health and socio-economic variables. Preliminary data show that the samples were similar in Epernon and the control towns and also comparable to some French epidemiological data. There is a striking difference between the percentage of subjects aware of their blood pressure (65.5%) and blood cholesterol (13.4%) levels.

Adult↗
PubMed1993

[Buerger disease, clinical and prognostic aspects. 83 cases].

A retrospective analysis of 83 records of patients with Buerger's disease is presented. There were 71 men and 12 (14.5 percent) women. Compared with men, women with Buerger's disease had a significantly more frequent vasomotor disorder, but they had less trophic disorders and a lower risk of amputation. After a 42-month follow-up, it appeared that tobacco plays a major role in the prognosis: patients who continued to smoke had significantly more numerous acute episodes than those who ceased smoking. The degree of intoxication is an element of prognosis, but good medical management contributes to reduction in the number of major amputations: only 5 patients (6 percent), all male, had a leg (4 cases) or a thigh (1 case) amputated.

Adult↗
PubMed1993

Changes in acid-base status of marathon runners during an incremental field test. Relationship to mean competitive marathon velocity.

Four top-class runners who regularly performed marathon and long-distance races participated in this study. They performed a graded field test on an artificial running track within a few weeks of a competitive marathon. The test consisted of five separate bouts of running. Each period lasted 6 min with an intervening 2-min rest bout during which arterialized capillary blood samples were taken. Blood was analysed for pH, partial pressure of oxygen and carbon dioxide (PO2 and PCO2) and lactate concentration ([la-]b). The values of base excess (BE) and bicarbonate concentration ([HCO3-]) were calculated. The exercise intensity during the test was regulated by the runners themselves. The subjects were asked to perform the first bout of running at a constant heart rate fc which was 50 beats.min-1 below their own maximal fc. Every subsequent bout, each of which lasted 6 min, was performed with an increment of 10 beats.min-1 as the target fc. Thus the last, the fifth run, was planned to be performed with fc amounting to 10 beats.min-1 less than their maximal fc. The results from these runners showed that the blood pH changed very little in the bouts performed at a running speed below 100% of mean marathon velocity (nu m). However, once nu m was exceeded, there were marked changes in acid-base status. In the bouts performed at a velocity above the nu m there was a marked increase in [la-]b and a significant decrease in pH, [HCO3-], BE and pCO2. The average marathon velocity (nu m) was 18.46 (SD 0.32) km.h-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1993

[Staphylococcus aureus endocarditis: an unusual clinical picture].

We describe an unusual presentation of bacterial endocarditis due to Staphylococcus aureus in a 50 year-old woman with mitral insufficiency. The disease began by a vascular purpura without fever and a digital embolism. The source of infection was anal ulcerations. Diagnosis of endocarditis was made possible by trans-oesophagus echocardiography but not by trans-thoracic echocardiography. The patient was successfully treated by surgery associated with antibiotherapy. This observation emphasizes the indications of surgery at the acute phase of endocarditis. The anal source of endocarditis is original, no other case has been found in the literature.

Echocardiography, Transesophageal↗
PubMed1993

Familial HDL deficiency due to marked hypercatabolism of normal apoA-I.

In this article, we describe a 46-year-old man with severe high-density lipoprotein (HDL) deficiency and his kindred. In the proband, HDL cholesterol and apolipoprotein (apo) A-I levels were 5 and 4.5 mg/dL, respectively. Xanthomata, xanthelasma, arcus corneae, and hepatosplenomegaly were not present. The proband had coronary artery disease, but it was impossible to state whether the HDL deficiency cosegregated with premature coronary artery disease in this kindred. Pedigree analysis was suggestive of a codominant familial disease. Polymerase chain reaction amplification of the apoA-I gene of the proband, followed by subcloning and sequencing, did not reveal any mutation in either the coding regions or intron-exon junctions. A kinetic study using deuterated leucine to endogenously label apoA-I was performed to elucidate the metabolic basis of the apoA-I deficiency. We demonstrated marked hypercatabolism of apoA-I in the proband, with a fractional catabolic rate more than 10 times faster than normal; the plasma residence time of apoA-I in the proband was only 0.38 day compared with 4.10 days in a control subject. The apoA-I production rate was also substantially decreased in the proband. The association of a normal apoA-I gene sequence with marked hypercatabolism of apoA-I is similar to that described in Tangier disease. However, except for the presence of mild, diffuse, corneal deposits, this patient had no evidence of the reticuloendothelial cholesterol deposition characteristic of Tangier disease. This study establishes that a form of severe hypoalphalipoproteinemia distinct from Tangier disease can be caused by marked hypercatabolism of a normal A-I apolipoprotein.

Apolipoprotein A-I↗
PubMed1992

Human lipoprotein lipase. Analysis of the catalytic triad by site-directed mutagenesis of Ser-132, Asp-156, and His-241.

Lipoprotein lipase (LPL) plays a central role in normal lipid metabolism as the key enzyme involved in the hydrolysis of triglycerides present in chylomicrons and very low density lipoproteins. LPL is a member of a family of hydrolytic enzymes that include hepatic lipase and pancreatic lipase. Based on primary sequence homology of LPL to pancreatic lipase, Ser-132, Asp-156, and His-241 have been proposed to be part of a domain required for normal enzymic activity. We have analyzed the role of these potential catalytic residues by site-directed mutagenesis and expression of the mutant LPL in human embryonic kidney-293 cells. Substitution of Ser-132, Asp-156, and His-241 by several different residues resulted in the expression of an enzyme that lacked both triolein and tributyrin esterase activities. Mutation of other conserved residues, including Ser-97, Ser-307, Asp-78, Asp-371, Asp-440, His-93, and His-439 resulted in the expression of active enzymes. Despite their effect on LPL activity, substitutions of Ser-132, Asp-156, and His-241 did not change either the heparin affinity or lipid binding properties of the mutant LPL. In summary, mutation of Ser-132, Asp-156, and His-241 specifically abolishes total hydrolytic activity without disrupting other important functional domains of LPL. These combined results strongly support the conclusion that Ser-132, Asp-156, and His-241 form the catalytic triad of LPL and are essential for LPL hydrolytic activity.

Amino Acid Sequence↗
PubMed1992

Met 358 to Arg mutation of alpha 1-antitrypsin associated with protein C deficiency in a patient with mild bleeding tendency.

The molecular defect responsible for a dramatic prolongation of all standard clotting tests discovered in a 15-yr-old boy has been identified. Initial investigations revealed the presence of an activated Factor X (Factor Xa) and thrombin inhibitor which copurified with alpha 1-antitrypsin (alpha 1-AT), thereby suggesting the occurrence of an alpha 1-AT variant similar to alpha 1-AT Pittsburgh. This was confirmed by dot-blot analysis and direct sequencing after amplification by the polymerase chain reaction. A G to T transition at nucleotide 10038 results in the substitution of Met to an Arg, converting alpha 1-AT into an Arg-Ser protease inhibitor (serpin) that inhibited thrombin and Factor Xa more effectively than antithrombin III. Surprisingly, there was no bleeding history in the proband. The common mutation Z, which may explain a reduced expression of the allele bearing the Arg 358 Met mutation, was not observed in the propositus' DNA. To exclude the presence of another mutation, the coding regions and intron/exon junctions were sequenced. No other mutation was found. Recently, the patient experienced his first hemorrhagic episode at the age of 17. The level of the abnormal inhibitor had increased twofold 2 mo before. The large decrease in protein C concentration may account for the mild bleeding tendency in this case, despite the presence of the alpha 1-AT Pittsburgh mutation. An abnormal protein C pattern was observed in patient's plasma, suggesting that the circulating deficiency might be due to a deleterious effect of the abnormal inhibitor on both intracellular processing and catabolism of protein C.

Base Sequence↗
PubMed1992

[Blood cholesterol and mortality].

Mortality rates vary with serum cholesterol levels: the causal nature of this relationship is studied by prospective studies (analysis of associations) and unifactorial primary prevention trials (experimentation to determine causality). In prospective studies all cause mortality is often increased at low and high cholesterol levels because of the inverse relationships of this factor with cardiovascular mortality (positive) and non-cardiovascular mortality (negative). Coronary death increases proportionally to serum cholesterol levels in all populations, including those with low cholesterol levels, in both sexes and at all ages. The relationship with cerebrovascular mortality seems to depend on the clinical feature: increased mortality rate due to cerebral haemorrhage in patients with low serum cholesterol and a positive correlation with cerebral thrombosis. Mortality due to cancers is generally negatively correlated to serum cholesterol levels with a significant increase in mortality in patients with a low serum cholesterol. This relationship often becomes less significant as the time between measurement and death increases. Mortality due to violent causes is not usually related to serum cholesterol. The multitude of possible causes of confusion makes any causal interpretation of data illusory. Experimentation by unifactorial primary prevention trials is essential for any etiological research but none of the trials performed to date was designed to analyse the effect of lowering serum cholesterol on global or coronary mortality.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

[Relations between HDL-cholesterol and cardiovascular diseases].

Many retrospective and prospective epidemiological studies have demonstrated an inverse relationship between HDL-cholesterol and coronary risk. The predictive value of HDL-cholesterol is observed both in asymptomatic subjects and those with a primary vascular event. Several genetic abnormalities may be responsible for low HDL cholesterol (under 100 mg/dl or 0.26 mmol/l) or for a less severe hypoalphalipoproteinaemia. Despite some very low values, these rare causes of HDL deficiency are not all atherogenic and serve to emphasize the complexity of HDL metabolism. The protective role of HDL is explained by a number of mechanisms such as their role in the reverse transport from the peripheral tissues to the liver, their anti-oxidant effect and the increase in prostacyclin levels. The correction of isolated hypoalphalipoproteinaemia by drugs is controversial, but associated hyperlipidaemic states would be an indication to use drugs which increase the HDl-cholesterol the most.

Apolipoprotein A-I↗
PubMed1992

[Role of triglycerides in cardiovascular diseases].

The role of triglycerides in cardiovascular disease is a controversial subject. Despite differences of opinion, present data allow a certain number of conclusions to be drawn. Hyperchylomicronemia is not associated with atherosclerosis, whereas type III hyperlipidemia is very atherogenic. These two abnormalities are, however, rare, and the majority of hypertriglyceridemias are, in practice, associated with increased very low density lipoproteins. Many epidemiological trials do not identify hypertriglyceridemia as an independent risk factor when the cholesterol and, in particular, the HDL cholesterol levels, are taken into consideration. Nevertheless, these results must be interpreted with caution as hypertriglyceridemia represents a very heterogeneous entity which is closely related to many factors which affect coronary risk (hypertension, insulin resistance, sedentarity, and even tobacco consumption). Therefore, hypertriglyceridemia and hypo-HDL-emia may be the result of the same primary abnormality; as the HDL-cholesterol level is more stable, it is the parameter which will be identified as a protective factor in epidemiological trials. The available data is insufficient to affirm that therapeutic lowering of triglycerides is accompanied by a reduced coronary risk because none of the large scale trials were designed to analyse this problem. Despite these epidemiological data, the measurement of serum triglyceride levels remains important in patients with hyperlipidemia.

Cholesterol, HDL↗
PubMed1992

[Serum cholesterol and cancer. Is there a causal relationship?].

Several studies have reported an inverse relationship between serum cholesterol levels and the risk of cancer, especially of the colon (Seven Countries, Framingham, Chicago studies, London Whitehall Study, Paris prospective study, New Zealand Maori, Honolulu Heart Study, Hypertension Detection and Follow-Up Program, ...). For example, in the Multiple Risk Factor Intervention Trial (361 662 men), the global mortality graph was J-shaped, higher at either side of the 4.6-5.1 mmol/l value of serum cholesterol. This increased mortality with lower serum cholesterol levels was due to increased numbers of death from cancer. However, when the relationship is studied with respect to the time elapsed between the cholesterol measurement and death from cancer, the relative risk of death in the lowest decile with respect to the average of the following deciles, decreases with the period between measurement of the serum cholesterol and time of death. The negative relationship between serum cholesterol and death by cancer, very significant for deaths occurring within the first 5 years, disappeared almost completely for deaths occurring after 5 years. Other trials designed mainly to examine cardiovascular risk, and concerning smaller numbers, have not demonstrated this inverse relationship between serum cholesterol and cancer. This negative relationship between serum cholesterol and cancer must be acknowledged. It is weak and concerns mainly colonic cancer, especially in men in the elderly age groups. Several explanations have been put forward: influence of the combination of factors, competition of risk of death by other causes, chance, alteration of normal biological function of the cell membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗