The pathophysiological basis of the destabilization of the clinical course in ischemic heart disease

The role of the coagulative blood system in initiation of acute coronary events was investigated on patients with different clinical forms of ischemic heart disease (IHD). The obtained results indicate that unstable angina (UA) and myocardial infarction (MI) are two independent forms of the acute IHD with distinct qualitative peculiarities. The most common feature of UA was an increase in the functional activity of platelets both in cases proceeded in MI and in uncomplicated cases. It means that these changes may be treated as the main pathogenic factor if UA but not as a mechanism of its transformation to MI. But high degree of the risk of MI development appears if these changes are combined with preceding significant disturbances in the haemostatic balance as a result of inhibition of the activity of anticoagulative and fibrinolytic blood systems. These data show that differentiation of the diagnosis between UA and MI in its initial stage and the choice of the treatment principles should be based on the careful investigation of the coagulative potential of blood and of its most important components.     

Exchange of K+ or Cs+ for Na+ induces local and long-range changes in the three-dimensional structure of the tryptophan synthase alpha2beta2 complex

Monovalent cations activate the pyridoxal phosphate-dependent reactions of tryptophan synthase and affect intersubunit communication in the alpha2beta2 complex. We report refined crystal structures of the tryptophan synthase alpha2beta2 complex from Salmonella typhimurium in the presence of K+ at 2.0 angstrom and of Cs+ at 2.3 angstrom. Comparison of these structures with the recently refined structure in the presence of Na+ shows that each monovalent cation binds at approximately the same position about 8 angstrom from the phosphate of pyridoxal phosphate. Na+ and K+ are coordinated to the carbonyl oxygens of beta Phe-306, beta Ser-308, and beta Gly-232 and to two or one water molecule, respectively. Cs+ is coordinated to the carbonyl oxygens of beta Phe-306, beta Ser-308, beta Gly-232, beta Val-231, beta Gly-268 and beta Leu-304. A second binding site for Cs+ is located in the beta/beta interface on the 2-fold axis with four carbonyl oxygens in the coordination sphere. In addition to local changes in structure close to the cation binding site, a number of long-range changes are observed. The K+ and Cs+ structures differ from the Na+ structure with respect to the positions of beta Asp-305, beta Lys-167, and alpha Asp-56. One unexpected result of this investigation is the movement of the side chains of beta Phe-280 and beta Tyr-279 from a position partially blocking the tunnel in the Na+ structure to a position lining the surface of the tunnel in the K+ and Cs+ structures. The results provide a structural basis for understanding the effects of cations on activity and intersubunit communication.     

Myopia associated with hyperbaric oxygen therapy

BACKGROUND: Hyperbaric oxygen therapy (HBOT) involves exposing patients to elevated oxygen pressures and concentrations for the treatment of soft tissue degenerative diseases. As side effects, some patients experience cataract development and/or a significant increase in myopia. SUBJECTS: Eight subjects participated in this project. All were receiving HBOT for health problems. METHODS: For all subjects, acuities and refractive error corrections were measured before and after HBOT sessions at the beginning, midpoint, and end of therapy. For four subjects, A-scan ultrasound and corneal curvature measurements were also made before and after selected HBOT sessions. In addition, susceptibility to free radical damage and indicators of actual damage were measured by blood analyses. During the first half of HBOT therapy, four subjects took placebo tablets; during the second half, antioxidant supplements were given. RESULTS: No subject showed significant acuity or refractive error changes produced by single HBOT sessions. Two of the 8 subjects showed significant increases in myopia over the 20 session course of HBOT. No corresponding changes were found in the ultrasound, corneal curvature, or blood analysis data. DISCUSSION: Theoretically, the increases in myopia could have been caused by lenticular refractive index changes resulting from oxidative damage to lens proteins. However, the biochemical assays used in this project did not predict which subjects were susceptible to increased myopia, nor did they demonstrate elevated levels of free radical activity in a subject who did experience an increase in myopia.     

The response regulator-like protein Pos9/Skn7 of Saccharomyces cerevisiae is involved in oxidative stress resistance

To assess the standard curves of pulsatility index (PI) in different segments of middle cerebral artery (MCA): initial segment (MI) and subcortical segment (M2); to determine the variation of the flow velocity waveforms (FVW) of the M1 and M2 segments of MCA in presence of fetal distress and to establish the possible correlation between the two segments of MCA. 50 normal pregnancies from 25 weeks of gestation to term and 20 pregnancy with alteration of fetal growth rate were investigated with serial records of the FVW of the M1 and M2 segments of the MCA and of the umbilical artery (UA) with a colour Doppler system. Severe fetal distress was associated to cerebral-placental ratio below 1 (C/P < 1). The perinatal outcome was established on the basis: 1) abnormal intrapartum CTG, 2) emergency cesarean section, 3) Apgar score at 1st and 5th minute after birth and 4) birth eight centiles. In normal pregnancy P1 of M2 was always higher than that of M1: therefore M2/M2 resulted below 1, with a maximum peak near 32 weeks of gestation. In presence of moderate fetal distress only P1 of M2 was reduced (M1/M2 > 1). It exists a significant difference of PI in M1 and M2 segments of fetal MCA during gestation: thus MCA so it is important to identify the tract of fetal MCA when recording its FVW. Moreover we suppose that an initial "cerebral sparing" effect exists in order to protect the cortex by the initial hypoxic injury: this is shown by a M1/M2 > 1. The progression of fetal distress results in a greater haemodynamic modification, the so called "brain sparing" which is usually present when C/P < 1.     

Various possible pathogenicity factors in Staphylococcus aureus (proceedings)

Parametric and symptomatologic studies of the EEG in large populations have served to define stages of maturation and criteria of "normality". The younger the subjects, however, the wider are the variations. In the first stage of life only massive cerebral lesions afford unquestionable EEG evidence: in evaluating dysrhythmias it is necessary to bear in mind their high incidence in normal subjects. Hence their meaning is to be understood only by prolonged longitudinal studies. The reference here is not only to diffuse or focal slow anomalies, but also to specific pathologic rhythms. The difficulty of interpreting such anomalies is particularly evident when epileptogenic potentials are found, since they may be signs of a lesion but their clinical correlations are uncertain. The concept of "masked epilepsy" must be rejected. Only the diagnoses of latent or proven epilepsy are admissible, and these epilepsies may be without direct relationship to the clinical, psychiatric or central nervous findings in the affected subject. Numerous genetic, afferential, emotional or biologic factors are involved in the development of non-lesional disorders. Accordingly, the EEG has only a minor contribution to make in the definition of mild focal or diffuse pathologic anatomy of the brain in the very young subject.