Standard Model Prediction for Direct CP Violation in K→ππ Decay.

We report the first lattice QCD calculation of the complex kaon decay amplitude A_{0} with physical kinematics, using a 32³×64 lattice volume and a single lattice spacing a, with 1/a=1.3784(68) GeV. We find Re(A_{0})=4.66(1.00)(1.26)×10(-7) GeV and Im(A_{0})=-1.90(1.23)(1.08)×10(-11) GeV, where the first error is statistical and the second systematic. The first value is in approximate agreement with the experimental result: Re(A_{0})=3.3201(18)×10(-7) GeV, while the second can be used to compute the direct CP-violating ratio Re(ϵ^{'}/ϵ)=1.38(5.15)(4.59)×10^{-4}, which is 2.1σ below the experimental value 16.6(2.3)×10(-4). The real part of A_{0} is CP conserving and serves as a test of our method while the result for Re(ϵ^{'}/ϵ) provides a new test of the standard model theory of CP violation, one which can be made more accurate with increasing computer capability.

Isospin splittings in the light-baryon octet from lattice QCD and QED.

While electromagnetic and up-down quark mass difference effects on octet baryon masses are very small, they have important consequences. The stability of the hydrogen atom against beta decay is a prominent example. Here, we include these effects by adding them to valence quarks in a lattice QCD calculation based on Nf=2+1 simulations with five lattice spacings down to 0.054 fm, lattice sizes up to 6 fm, and average up-down quark masses all the way down to their physical value. This allows us to gain control over all systematic errors, except for the one associated with neglecting electromagnetism in the sea. We compute the octet baryon isomultiplet mass splittings, as well as the individual contributions from electromagnetism and the up-down quark mass difference. Our results for the total splittings are in good agreement with experiment.

Ab initio determination of light hadron masses.

More than 99% of the mass of the visible universe is made up of protons and neutrons. Both particles are much heavier than their quark and gluon constituents, and the Standard Model of particle physics should explain this difference. We present a full ab initio calculation of the masses of protons, neutrons, and other light hadrons, using lattice quantum chromodynamics. Pion masses down to 190 mega-electron volts are used to extrapolate to the physical point, with lattice sizes of approximately four times the inverse pion mass. Three lattice spacings are used for a continuum extrapolation. Our results completely agree with experimental observations and represent a quantitative confirmation of this aspect of the Standard Model with fully controlled uncertainties.

[Evaluation of management of infarction in the Franche Comté province by the use of the Franche Comté Cardiology Registry, May 2005-May 2006]. / L'évaluation des pratiques professionnelles pour la prise en charge des infarctus en Franche-Comté. Expérience d'une évaluation à l'échelle régionale par l'utilisation des données du registre franc-comtois de cardiologie, mai 2005-mai 2006.

RATIONALE: The management of acute infarction often necessitates a network of organisation between different centres, thus making it the object of an evaluation of professional practices (EPP). We report the experience in the Franche Comté province of an EPP at a regional level in the management of infarction. METHODS: All of the patients admitted to 10 of the 11 centres in the region were included in a prospective survey. Quality indicators for acute and chronic care were defined, as well as scores, on the basis of use of treatments specified in guidelines. RESULTS: Between May 2005 and May 2006, 1,170 patients were admitted. The patients' risk levels and quality scores were calculated. The rate of use of the quality indicators was higher in our survey than that observed in all of the published studies, except for the use of betablockers. The quality of care could therefore be considered as highly satisfactory. Comparison between the centres revealed some differences. Even after adjustment for the risk score on admission, the quality score for acute care was related to mortality at 1 month. CONCLUSIONS: An EPP is possible for the management of infarction, on a regional scale such as in the province of Franche Comté. The acute quality score turned out to be an independent factor for mortality. The indicators showed that the quality of care was highly satisfactory, even though more progress could be made in the prescription of betablockers.

[Results of high amplification electrocardiogram in primary dilated cardiomyopathy]. / Résultats de l'électrocardiogramme haute amplification dans la cardiomyopathie dilatée primitive.

Idiopathic dilated cardiomyopathy carries a high risk of sudden death. It is also associated with sustained ventricular tachycardia. A complex ventricular arrhythmia is recorded in 3/4 of cases on Holter monitoring which has a low specificity. The aim of the study was to determine whether signal-averaged electrocardiography could provide a better evaluation of the prognosis of this condition. The results of signal-averaged electrocardiography were compared with those of 24 hour Holter monitoring and of systematic programmed ventricular stimulation in 58 patients with idiopathic dilated cardiomyopathy. Late ventricular potentials were recorded in 13 of the 14 subjects with inducible and usually spontaneous sustained ventricular tachycardia. The sensitivity of the technique for evaluating the risk of sustained VT was therefore good (93%). Late potentials were also recorded in 9 patients with induced ventricular flutter or fibrillation, these patients being symptomatic (dizzy spells). Late potentials were also demonstrated in 14 of the 35 asymptomatic patients without inducible VT, indicating that this non-invasive investigation had a limited specificity (60%). In addition, during follow-up of the patients, the risk of sudden death was difficult to demonstrate. Late potentials were only found in subjects with inducible sustained VT but no in the other cases. In conclusion, signal-averaged electrocardiography seems to be valuable for evaluating the risk of sustained VT in subjects with idiopathic dilated cardiomyopathy and complex ventricular arrhythmias. The detection of the risk of sudden death is probably impossible by this technique.

[Primary hyperlipoproteinemia in childhood (author's transl)]. / Hiperlipoproteinemia primaria tipo V en el niño.

Type V hyperlipoproteinemia is an unusual entity in children. Only 6 cases have been described so far to our knowledge. Authors present a 9 year old male that came for diagnosis of a hepatosplenomegaly. There was no evidence of abdominal pain, xanthomas or pancreatitis. Secondary disorders such as uncontrolled insulinopenic diabetes mellitus, glycogen storage disease, administration of estrogen compounds, nephrotic syndrome or uremia, and dysglobulinemias were excluded. His father presented the same lipoprotein pattern suggesting a dominant mode of inheritance. The administration of heparin showed a good response of serum proteinlipase.

[Hypokalemic periodic paralysis. Report of two cases (author's transl)]. / Estudio de dos casos de parálisis periódica hipopotasémica.

The familial periodic hypokalemic paralysis is an infrequent disease characterized by paralytic attacks of sudden appearance affecting the muscles of the trunk and limbs. There is a marked hypokalemia during the paralytic episodes of the disease, and a family history in 80 percent of the cases. The differential diagnosis includes hyperthyroidism with periodic paralysis, congenital paramyotony and adynamia episodica hereditaria. Two typical cases of hypokalemic periodic paralysis are presented, with biological, electrophysiological, clinical, and ultrastructural pictures characteristics of the disease. The clinical manifestations of both patients are discussed, stressing the diagnostic importance of the electrophysiological study during the insulin test, and the interest of the histologic and ultrastructural studies. The spectacular response during the acute episodes to the intravenous perfusion of potassium salts, and the usefulness of the acetazolamide administration to prevent the paralytic episodes are emphasized.

[Bile acids. I. Nature, physiology, and functions (author's transl)]. / Acidos biliares. I. Naturaleza, fisiología y funciones.

Bile acids play a fundamental role in the degradation and absorption of intestinal lipids. The primary ones are cholic acid and chenodeoxycholic acid which are synthesized from cholesterol in the liver and conjugate with taurine and glycine amino acids. The secondary bile acids are derived from the primary ones by the enzyme action of intestinal bacteria through a process of deconjugation and dehydroxylation. Their detergent property is based on the molecular configuration of these compounds, which present a hydrophilic and a hydrotion of these compounds, which present a hydrophilic and a hydrophobic surface. The different enzymes in the liver cells that intervene in the process of synthesis of bile acids are now known. A basic element in their physiology is the enterohepatic circulation, enabling the organism to take maximum advantage of these compounds. The dynamics of the cycle are maintained and regulated by the system of uptake and secretion of the cells, cholecystokinin, intestinal peristalsis, active transport across the ileal membrane, and by portal venous flow. Much of our knowledge about the biogenesis and functions of the bile acids has been acquired quite recently. Research over the past three decades has contributed to a great advance in our understanding of their physiology.

[Bile acids II. Physiopathologic and clinical aspects (author's transl)]. / Acidos biliares. II. Aspectos fisiopatológicos y clínicos.

It is generally accepted that the bile acids are responsible for pathologies as a result of deficiency or by toxic action. Quantitative deficiency is difficult to evaluate but the normal pool of bile acids is generally considered to be between 2 and4 grams. Daily loss and replacement by synthesis is thought to be between 500 and 700 mg. There is experimental evidence to demonstrate the toxic action of certain bile acids on metabolic structures and processes. There is no doubt that alterations in the metabolism of bile acids give rise to certain pathologic aspects in some diseases of the gastrointestinal tract or the hepatobiliary system. There are other conditions, on the other hand, in which the study of these acids may reveal significant physiopathologic implications. The first group includes terminal ileopathy, blind loop syndrome, gastric ulcer, gastritis, cholestasis, cirrhosis of the liver, and cholelithiasis. In the second group are such diverse conditions as acute pancreatitis, cancer of the colon, endocrine disturbances, some hyperlipidemias, and others. Much of the present day understanding of the physiopathology of the bile acids will probably have to be revised in the nex few years, in view of the rapid advances being made in this field.

In vivo and in vitro relationship between lipoprotein-X and bile salts in cholestasis.

Bile salts have been shown to act on lipoprotein-X (LP-X) in vitro to induce a false-negative electrophoretic test. The aim of the present study was to investigate the relationship between serum LP-X and serum bile acids in patients with cholestasis. The in vitro concentration of bile salts required to induce a negative or reduced concentration of LP-X was also studied. There was no relationship, either positive or negative, between serum LP-X and bile acids in 34 patients with cholestasis. Serum was incubated with various saline solutions of taurocholic, lithocholic, deoxycholic and glycocholic acids. The concentration of LP-X decreased only after the final concentrations of bile salts were over 2,000 mumole/1. This is more than five times the concentration of serum bile salts usually found in patients with cholestasis. It is concluded that the negative LP-X test in some patients with cholestases must be explained by some other mechanisms than bile salts.

Liver tissue lecithin: cholesterol acyltransferase activity in patients with liver disease.

Lecithin: Cholesterol acyltransferase (LCAT) activity was measured in serum and liver tissue from patients with parenchymal liver disease. Serum LCAT activity was within normal limits and it was probably related to the absence of clinical and laboratory evidence of a decompensated liver function. Liver tissue LCAT activity is about tenfold lower than that in serum. The relative proportion of cholesterol esters in liver tissue was much higher that could be expected according the low tissue LCAT activity. This findings suggest that LCAT is a "plasma specific" enzyme and that cholesterol esters in parenchyma may be considered as a storage form of cholesterol esterified in plasma pool.