The ATP synthase of Trypanosoma brucei is developmentally regulated by an inhibitor peptide

The Trypanosoma brucei ATP synthase, like those of other organisms, is composed of two moieties, the membrane bound F0 and the catalytic F1 with each of these parts comprised of multiple subunits. In addition, an endogenous inhibitor peptide of the ATP synthase has been identified from a variety of sources. Previous reports have suggested that the Trypanosoma brucei ATPase may not possess such an inhibitor. Recently, we have isolated an inhibitor peptide fraction from the procyclic form of Trypanosoma brucei by modification of a previously published procedure. This fraction is composed of two dominant polypeptides with estimated molecular weights of 14,000 and 12,000 and an additional polypeptide of 15,000 that may or may not be functionally required. Antibodies raised to the smallest polypeptide showed strong cross reactivity with the other two polypeptides, suggesting that they are related. Antibodies to rat liver inhibitor peptide show cross reactivity with the same polypeptides in crude fractions. The inhibitor peptide fraction strongly suppresses the ATPase activity of membrane bound ATPase in a Mg(2+)-dependent manner and is cold and heat stable. Using antibodies to the smallest polypeptide and rat liver inhibitor peptide we have shown in crude extracts from the three experimental life cycle stages of T. brucei that the inhibitor peptide(s) is developmentally regulated to a modest extent. The pattern of regulation is opposite of the pattern seen for the ATP synthase complex. This suggests that the ATP synthase is stringently controlled in T. brucei in a unique way.     

Continuous monitoring of global left ventricular ejection fraction during percutaneous transluminal coronary angioplasty

Continuous monitoring of left ventricular (LV) function during percutaneous transluminal coronary angioplasty (PTCA) was performed in 40 patients (53 +/- 2 years) with a miniature, nuclear detector system after labeling the patients' red blood cells with technetium-99m. Balloon dilation (113 seconds, range 60 to 240) induced on average a 0.12 ejection fraction (EF) unit (19%) decrease in the LVEF, which was explained by a 34% increase in end-systolic counts. Balloon dilation of the left anterior descending artery (n = 23) produced a decrease in the LVEF of 0.17 +/- 0.13 EF units compared with the decrease of 0.06 +/- 0.07 EF units in patients undergoing dilation of the left circumflex artery (n = 9) and 0.05 +/- 0.04 EF units in patients treated for a stenosis of the right coronary artery (n = 8), (p = 0.02). Balloon deflation was associated with an immediate return to pre-PTCA levels. In 10 patients with 2 identical balloon occlusions, the second occlusion led to a significantly less decrease in the LVEF (0.41 +/- 0.14 vs 0.44 +/- 0.15) and electrocardiographic ST-segment deviation (88 +/- 54 microV vs 65 +/- 42 microV) than the first. We conclude that PTCA is associated with an abrupt transient decrease in the LVEF. The effect of balloon occlusion of the left anterior descending artery is more pronounced than balloon occlusion of the left circumflex and the right coronary arteries. Neither single nor multiple balloon occlusions were associated with post-PTCA global LV dysfunction, whereas the lesser degree of LV dysfunction and electrocardiographic signs of myocardial ischemia during the second of 2 identical balloon occlusions suggests that preconditioning can be induced during PTCA.     

Platelet adhesion, release and aggregation in flowing blood: effects of surface properties and platelet function

Platelet adhesion to natural and artificial surfaces and adhesion-induced aggregation were investigated in vitro using an annular perfusion chamber. The surfaces were exposed to anticoagulated blood under identical flow conditions (approximately arterial shear rates). The initial attachment of platelets (contact) appeared less surface specific than spreading and release. Fibrillar collagen was the most powerful inducer of platelet degranulation whereas elastin, microfibrils and epon were virtually inactive. Fibrillar collagen caused release also in the absence of spreading. Surface coverage with platelets did not exceed 25% unless spreading occurred. Perfusion with platelet-free plasma or platelet-poor blood did not remove adhering platelets. However, platelets were translocated from mural thrombi to the surface by such perfusion. In addition, platelets which detached from mural thrombi adhered more readily to elastin or microfibrils than platelets from the circulating blood. The initial attachment of platelets to subendothelium was inhibited in von Willebrand's disease, the Bernard-Soulier syndrome and at high concentrations of dipyridamole; spreading was inhibited in storage pool disease of rats, at low temperature (20 degrees C), with EDTA (3 MM) and Prostaglandin E1 (1 muM); and adhesion-induced aggregation was inhibited in thrombasthenia, storage pool disease and after ingestion of sulfinpyrazone or Aspirin. It is concluded that the initial attachment (contact) of platelets, spreading and surface-induced release of platelet constituents are at least partially indendent phenomena, the latter two being highly surface specific. At flow conditions which cause the disappearance of platelet adhesion appears as an irreversible process.     

Supporting the free exercise of religion in the group home context

Ways were delineated in which group home employees can support individuals living in the home in the active expression of faith, both inside and outside the group home environment, and at the same time protect the freedom of others in the home who choose not to be involved in religious activities. After briefly reviewing some assumptions underlying the 1992 AAMR definition of mental retardation and describing the capability of religious expression for individuals with cognitive impairment, we presented several guidelines to assist group home staff members.     

Circadian rhythm in plasma concentrations of gamma-hydroxybutyric acid in alcoholics

Gamma-hydroxybutyric acid (GHB) was orally administered to six alcoholics at 09.00 and 23.00 h. The plasma concentrations of GHB show a clear circadian pattern, the area under the curve in the daytime experiments being 61% of that in the night experiments. The significance of alcohol dehydrogenase, the catabolic enzyme of GHB, for the difference is discussed. It is concluded that, although the activity of alcohol dehydrogenase in alcoholics is quantitatively disturbed, it remains subject to physiologic circadian activation.     

Immune parameters in athletes before and after strenuous exercise

Secretory IgA levels were studied in nationally ranked Nordic skiers before and after the national cross-country races held in February 1981. Comparing the skiers with age-matched controls, there was significantly lower level of salivary IgA before the race. Concentrations of IgA decreased further following the competition (50 kn for males; 20 km for females) to very low levels. There also were a significant increase in the percentage of B lymphocytes and a decrease in the null population (non-T, non-B) in the athletes after the race compared with the controls. The mechanism responsible for these changes is unknown, but the low salivary IgA levels may result from depletion of nasal fluid and/or malfunction of the mucosal plasma cells due to a decrease temperature in the mucous membranes. We speculated that a temporary antibody deficiency on the mucosal surface might lead to a susceptibility to acquiring viral and bacterial infections, especially during the interval immediately following strenuous exercise.