Ocular manifestations of dysproteinemias APPELMANS, M; MICHIELS, J; MASSA, J M ...
Archives d'ophtalmologie et revue generale d'ophtalmologie
22
Journal Article
The influence of auto-oxidized phospholipids on the reduction of the tetrazolium salt MTT coupled to the NAD+-dependent lactate dehydrogenase reaction was studied. The following results were ...obtained: (1) peroxidized phosphatidylcholine interfered in the time-course of the lactate dehydrogenase-mediated MTT reduction; (2) there was a time-dependent decrease in the hydroperoxide content of phosphatidylcholine vesicles during the incubation; (3) the diminution of phosphatidylcholine hydroperoxides required the presence of all the components of the system except MTT; (4) hydroperoxide diminution and MTT reduction were mediated by the superoxide radical O2-, since both processes were inhibited by superoxide dismutase; (5) EDTA inhibited the hydroperoxide decrease and abolished the interference of peroxidized phosphatidylcholine with MTT reduction. It was concluded that hydroperoxides compete with MTT for the electrons coming from substrate oxidation. The superoxide radical O2- and traces of some contaminating metal ion are involved in the process. This is a potential complication in the study of the effect of lipids on enzymatic activities assayed by the tetrazolium salt method.
A 6a-(3′,4′-dichlorophenylamino) analog of viomycin was uncovered by a high-throughput screen against the animal health pathogen
Pasteurella haemolytica, and has served as a novel lead structure for ...our infectious disease programs. We report herein the synthesis and activity of analogs of tuberactinomycins and capreomycin that are active against
Pasteurella spp., methicillin-resistant
Staphylococcus aureus, and vancomycin-resistant enterococci.
This paper describes the synthesis and activity of some C-6a-substituted analogs of tuberactinomycins and capreomycin, which are active against
Pasteurella spp., methicillin-resistant
Staphylococcus aureus, and vancomycin-resistant enterococci.
Trials were conducted with an ohmic heating pilot plant in order to ascertain the extent of metal release from the electrodes under different conditions of current frequency (50 and 25,000 Hz). The ...trials were performed with solutions having different aggressiveness: hydrochloric acid and sodium chloride, hydrochloric acid, citrate buffer and sodium chloride and citrate buffer. The results show that, apart from solution aggressiveness, metal releases are negligible at the 25,000 Hz frequency. At 50 Hz, metal releases increase with increasing solution aggressiveness, reaching very high levels
Sono state condotte prove con un impianto pilota di riscaldamento ohmico allo scopo di verificare l'entita' delle cessioni di metalli da parte degli elettrodi in condizioni diverse di frequenza della corrente (50 e 25.000 Hz). Le prove sono state condotte con soluzioni a diversa aggressivita': acido cloridrico e cloruro di sodio, acido cloridrico, tampone citrato e cloruro di sodio e tampone citrato. I risultati mostrano che, indipendentemente dall'aggressivita' della soluzione, alla frequenza di 25.000 Hz le cessioni sono trascurabili. A 50 Hz le cessioni di metalli aumentano con l'aggressivita' della soluzione, raggiungendo livelli assai elevati
Noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonists, including ketamine, MK-801, and phencyclidine (PCP), induce the HSP70 heat shock or stress gene in pyramidal neurons in rat posterior ...cingulate and retrosplenial cortex. PCP also induces HSP70 in many other pyramidal neurons in brain including neocortex, insular cortex, piriform cortex, hippocampus, and basal nuclei of the amygdala. Several neurotransmitter antagonists, including haloperidol, clozapine, SCH-22390, diazepam, and muscimol, inhibited induction of HSP70 produced by PCP. Baclofen had no effect. Nifedipine blocked induction of HSP70 by PCP in cingulate, neocortex, and insular cortex but only partially blocked HSP70 in piriform cortex and amygdala. These data suggest that phencyclidine injures pyramidal neurons via dopamine D1, D2, D4, sigma, and other receptors. Gamma-aminobutyric acid (GABA) agonists ameliorate the injury. A model is proposed whereby NMDA receptor blockade on GABA neurons decreases inhibitory inputs onto cortical pyramidal neurons and makes them more vulnerable to injury from a variety of excitatory inputs. It is possible that psychosis produced by PCP and other NMDA antagonists correlates with overactivity and eventual injury to cingulate pyramidal neurons.
Surface-modifying macromolecules (SMMs) are fluorinated oligomers that are immiscible in polyurethanes and migrate to the surface of polyurethane blends, forming a hydrophobic surface that minimizes ...non-specific biological interactions. Three different SMMs (PPO212L, PTMO212F and PTMO212I) were used to surface modify a polyetherurethane (Base PU) and were shown to reduce the number of adherent platelets in previously reported work. However, higher levels of platelet activation were observed on the Base PU and PTMO212I surfaces as measured by scanning electron microscopy and image analysis. In the current thesis, it was hypothesized that the nature of platelet activating proteins, such as fibrinogen, was modulated on these surfaces. Therefore, the nature of the adsorbed fibrinogen (Fg) was investigated to explain the platelet response. The quantity of adsorbed Fg measured from buffer, human plasma and reconstituted whole blood could not account for the platelet number because protein adsorption yielded similar Fg levels on all surfaces. The Fg distribution and platelet activation were highly correlated at larger platelet aggregate ranges. The Fg antibody detection showed that the presentation of the Fg molecule, represented by conformation, orientation and molecule packing, drives platelet response (attachment and activation). More specifically, the data highlight the domain "communication" within the Fg molecule, which responds to different surfaces, and directs platelet response. Upon AFM analysis of hydrated surfaces, it was found that the PPO212L and PTMO212F materials had a well-mixed phase structure and the lowest platelet adhesion, platelet activation, Fg aggregate size and antibody detection. Conversely, Base PU and PTMO212I materials had isolated phases (large rounded vs. striated, respectively) and had higher platelet activation, Fg aggregates and antibody detection. The conclusion was that SMMs could be formulated to modulate Fg in a manner that reduced platelet activation in blood contacting PUs.
To determine the proportion of patients with myocardial infarction (MI) not admitted to a coronary care unit (CCU), the variables associated with admission into a CCU, and whether admission to a CCU, ...and the availability of coronary angiography in the same hospital, were associated with 28-day case fatality.
Population-based registry of MI in patients 25 to 74 years of age, admitted during 1996-1998. Demographic and clinical characteristics were recorded, as well as management, clinical course and survival after 28 days. Hospitals were classified according to the availability of a CCU and catheterization laboratory (advanced hospital), CCU only (intermediate hospital) or neither (basic hospital). Admission to the CCU was also recorded.
In all, 9046 cases of MI were recorded; in 11.3% the patient was not admitted to a CCU. Age, smoking (OR=1.33; 95% CI, 1.08-1.64), non-Q MI (OR=0.62; 95% CI, 0.49-0.78) or undetermined location of MI (OR=0.34; 95% CI, 0.23-0.50), Killip 4 score on admission (OR=0.63; 95% CI, 0.40-1.00) and delay in arrival at the hospital >6 h were associated with CCU admission. Patients admitted to a CCU showed a lower case fatality in the first 24 h (4.2% vs 23.5%), which was independent of comorbidity, severity and treatment. The 24-hour survivors admitted to a basic hospital had higher case fatality (17.3% vs 7.8%) than other groups, which was related to differences in treatment.
CCU admission is associated with a lower case fatality in the first 24 h. Admission to a basic hospital is associated with a higher 28-day case fatality even in patients who survive 24 h.
Determinar el porcentaje de pacientes con infarto agudo de miocardio (IAM) que no ingresan en una unidad de cuidados intensivos coronaries (UCIC), las variables asociadas al ingreso en una UCIC y si el ingreso en una UCIC, su disponibilidad y la de hemodinámica en el hospital se asocian a la letalidad a 28 días.
Registro poblacional (1996-1998) de casos de IAM en pacientes con edades comprendidas entre los 25 y los 74 años. Se recogieron variables demográficas, clínicas, el ingreso en UCIC y la letalidad a los 28 días. Se clasificaron los hospitales según la disponibilidad de UCIC y hemodinámica (hospital avanzado), solamente UCIC (hospital intermedio) o ninguno (hospital básico).
Se registraron 9.046 casos; el 11,3% no ingresó en una UCIC. La edad, el consumo de tabaco (
odds ratio OR = 1,33; intervalo de confianza IC del 95%, 1,08-1,64), el infarto sin onda Q (OR = 0,62; IC del 95%, 0,49-0,78) o ilocalizable (OR = 0,34; IC del 95%, 0,23-0,50), el grado Killip 4 al ingreso (OR = 0,63; IC del 95%, 0,40-1,00) y el retraso > 6 h en llegar al hospital se asociaron al ingreso en UCIC. Los pacientes ingresados en UCIC presentaban menor letalidad que los ingresados en hospitales básicos en las primeras 24 h (el 4,2 frente al 23,5%), independientemente de la gravedad del IAM y de las variables relacionadas con el tratamiento. Los su-pervivientes a 24 h que ingresaban en un hospital bÁsico presentaban mayor letalidad a los 28 días (el 17,3 frente al 7,8%), relacionada con las variables de tratamiento.
El ingreso en una UCIC se asocia a una menor letalidad de los pacientes con IAM en las primeras 24 h. El ingreso en un hospital bÁsico se asocia a una mayor letalidad a los 28 días.
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